CD86 Antibody, Biotin

What is CD86 and why would I use a biotinylated antibody to study it?

CD86, also known as B7-2, is an approximately 80 kDa surface receptor belonging to the B7 family of costimulatory molecules. It is a type I membrane protein and member of the immunoglobulin superfamily primarily expressed by antigen-presenting cells (APCs) . CD86 serves as a counter-receptor for the T cell surface molecules CD28 and CD152 (CTLA-4), playing a crucial role in T-B crosstalk and immune response regulation . Biotinylated antibodies provide exceptional versatility in research applications due to biotin's high affinity for streptavidin and avidin. This characteristic allows for signal amplification in detection systems and enables flexible experimental protocols where secondary detection reagents can be varied while maintaining consistent primary antibody binding. For CD86 detection, biotinylated antibodies are particularly useful in flow cytometry applications, allowing researchers to examine expression patterns on various cell populations with high sensitivity .

How does CD86 function in the immune system?

CD86 functions as a critical costimulatory molecule in the immune system, participating in the "second signal" required for effective T cell activation. During antigen presentation, CD86 on APCs interacts with CD28 on T cells, providing essential costimulatory signals that promote T cell proliferation, cytokine production, and survival . This interaction is particularly important during the primary phase of an immune response due to the rapid upregulation kinetics of CD86 following stimulation . Conversely, CD86 binding to CTLA-4 (CD152) on activated T cells delivers inhibitory signals that negatively regulate T cell activation and help diminish the immune response, contributing to immune homeostasis . CD86 also plays important roles in T-B cell collaboration, autoantibody production, and Th2-mediated immunoglobulin production . The absence of sufficient CD86-mediated costimulation during antigen presentation can induce immune tolerance rather than activation, highlighting its significance in shaping appropriate immune responses .

Which cell types express CD86 and how is its expression regulated?

CD86 is expressed primarily by professional antigen-presenting cells including:

• B cells (low basal level, highly inducible)

• Macrophages (low basal level)

• Dendritic cells (low basal level)

• Activated mouse T cells (species-specific expression)

• Thioglycolate-elicited peritoneal cells in mice

CD86 expression is tightly regulated and can be upregulated through various stimuli. On B cells, upregulation occurs through several pathways including BCR complex signaling, CD40 engagement, and cytokine receptor activation . The kinetics of CD86 upregulation make it particularly important during the primary phase of immune responses, as it can be rapidly expressed following stimulation . This dynamic regulation allows for precise control of costimulatory signals during different phases of immune responses. Flow cytometric analysis is commonly used to detect and quantify CD86 expression on these cell populations, with antibodies such as IT2.2 (human-specific) or GL1 (mouse-specific) being valuable tools for these studies .

What is the difference between CD86 (B7-2) and CD80 (B7-1) in immune responses?

While CD86 (B7-2) and CD80 (B7-1) are both members of the B7 family of costimulatory molecules and share the same binding partners (CD28 and CTLA-4), they exhibit important functional and expression differences:

CD86 appears to play a role distinct from CD80 in T helper cell differentiation, suggesting non-redundant functions in shaping immune responses . Both molecules can provide costimulation, but their differential expression patterns and binding properties allow for fine-tuning of immune activation and regulation at different stages of the response . The rapid upregulation of CD86 upon stimulation supports its major contribution during the primary phase of an immune response, whereas CD80 may play more prominent roles in later stages .

What is the recommended concentration of biotinylated CD86 antibody for flow cytometry?

The optimal concentration of biotinylated CD86 antibody for flow cytometry depends on the specific clone and application. Based on manufacturer recommendations:

• For the IT2.2 monoclonal antibody (human-specific): Use ≤0.5 μg per test

• For the GL1 monoclonal antibody (mouse-specific): Use ≤0.25 μg per test

A "test" is defined as the amount of antibody required to stain a cell sample in a final volume of 100 μL . The number of cells can range from 10^5 to 10^8 cells per test, though this should be empirically determined for each experimental system . It is strongly recommended to carefully titrate the antibody for optimal performance in your specific assay to achieve the best signal-to-noise ratio. This involves testing several antibody concentrations with the same cell samples to determine the concentration that provides maximum specific staining with minimal background. Proper titration not only ensures reliable results but also helps conserve valuable reagents and maximize the number of experiments possible with limited antibody supplies .

How should I prepare my samples for optimal CD86 detection?

For optimal CD86 detection using biotinylated antibodies, follow these methodological guidelines:

• Cell preparation:

  • For peripheral blood samples: Use fresh samples or properly cryopreserved cells

  • For cultured cells: Ensure viability >90% for reliable results

  • Adjust cell concentration to 1-5 × 10^6 cells/mL in appropriate buffer

• Staining protocol for flow cytometry:

  • Prepare single-cell suspensions in cold buffer (PBS + 1-2% FBS/BSA)

  • Block Fc receptors to reduce non-specific binding (10-15 minutes incubation)

  • Add titrated amount of biotinylated CD86 antibody (≤0.5 μg for IT2.2; ≤0.25 μg for GL1)

  • Incubate 20-30 minutes at 2-8°C protected from light

  • Wash cells twice with staining buffer

  • Add appropriate streptavidin conjugate (fluorophore of choice)

  • Incubate 15-20 minutes at 2-8°C protected from light

  • Wash twice and resuspend in appropriate buffer for analysis

• Sample considerations:

  • For activated samples: Culture cells with appropriate stimuli (LPS for dendritic cells, anti-IgM or CD40L for B cells)

  • Monitor viability with appropriate exclusion dyes

  • Consider cell fixation if analysis will be delayed

Remember that CD86 expression is typically low on resting cells and increases following activation, so including both resting and activated samples can provide important biological controls . The staining protocol may need optimization based on your specific application and cell type.

What controls are critical when using biotinylated CD86 antibodies?

When using biotinylated CD86 antibodies, including proper controls is essential for accurate data interpretation:

• Isotype controls:

  • Include appropriate biotinylated isotype control antibodies matched to the primary antibody's host species and immunoglobulin class (e.g., biotinylated rabbit IgG for rabbit polyclonal antibodies)

  • Apply the same concentration as the CD86 antibody

  • This helps distinguish non-specific binding from genuine CD86 detection

• Biological controls:

  • Positive controls: Include cell populations known to express CD86 (e.g., activated B cells, dendritic cells)

  • Negative controls: Include cell populations known to lack CD86 expression

  • Activation controls: Compare resting vs. activated populations to confirm expected upregulation patterns

• Technical controls:

  • Unstained cells: To establish autofluorescence baseline

  • Secondary-only controls: Cells treated with streptavidin conjugate only (no primary antibody)

  • Fluorescence minus one (FMO) controls: In multicolor panels, include samples with all fluorophores except the one detecting CD86

  • Single-stained controls: For compensation setup in multicolor experiments

• Validation controls:

  • Cross-validation with another CD86 antibody clone or detection method

  • Blocking controls: Pre-incubation with unconjugated antibody should reduce specific staining

Implementing these controls helps ensure reliable and interpretable results when studying CD86 expression patterns in your experimental system.

Should I choose a monoclonal or polyclonal CD86 antibody for my experiment?

The choice between monoclonal and polyclonal CD86 antibodies depends on your specific research needs:

Consider monoclonal antibodies when:

• You need high specificity and consistent results across experiments

• You're performing flow cytometry applications

• You're focusing on a single species (human or mouse)

• You want to target a specific CD86 epitope

Consider polyclonal antibodies when:

• You need to detect CD86 across multiple species

• You require versatility across different experimental techniques

• You want to maximize detection of all CD86 protein variants

• You're performing Western blot or immunohistochemistry experiments

How can I use CD86 antibodies to investigate T cell-APC interactions?

Biotinylated CD86 antibodies are valuable tools for studying the complex dynamics of T cell-APC interactions:

• Co-culture systems analysis:

  • Use flow cytometry to simultaneously measure CD86 expression on APCs and activation markers on T cells

  • Track temporal changes in CD86 expression during APC-T cell interactions

  • Correlate CD86 expression levels with T cell proliferation and cytokine production

• Blocking experiments:

  • Use non-biotinylated CD86 antibodies to block CD86-CD28/CTLA-4 interactions

  • Compare with isotype controls to determine the specific contribution of CD86 to T cell activation

  • Assess downstream effects on cytokine production, proliferation, and effector function

• Imaging applications:

  • Utilize biotinylated CD86 antibodies with streptavidin-fluorophore conjugates for immunofluorescence

  • Examine the spatial distribution of CD86 at the immunological synapse

  • Combine with other markers to visualize receptor clustering and signaling complex formation

• Functional assays:

  • Measure CD86 expression before and after specific APC activation stimuli

  • Correlate CD86 upregulation with functional outcomes in T cell responses

  • Investigate how CD86 contributes to differential T helper cell polarization

These approaches help elucidate the critical role of CD86 in providing costimulatory signals that determine whether T cells become fully activated or develop tolerance in response to antigen presentation. The interactions between CD86 on APCs and CD28/CTLA-4 on T cells are fundamental to understanding immune regulation mechanisms and developing immunotherapeutic strategies .

What are the best approaches for studying CD86 in costimulatory signaling pathways?

To investigate CD86's role in costimulatory signaling pathways:

• Receptor engagement studies:

  • Use CD86 antibodies to track receptor expression before and after CD28/CTLA-4 engagement

  • Analyze changes in CD86 distribution and phosphorylation status following ligand binding

  • Investigate bidirectional signaling where CD86 not only activates T cells but may also transduce signals back to APCs

• Signaling pathway analysis:

  • Combine CD86 detection with phospho-flow cytometry to measure activation of downstream signaling molecules (NF-κB, MAPK, PI3K)

  • Use CD86 blockade to determine which signaling pathways are dependent on CD86-mediated costimulation

  • Examine how CD86 signaling integrates with other costimulatory pathways

• Genetic approaches:

  • Use CD86 knockout or knockdown systems to evaluate its necessity in costimulatory signaling

  • Re-express wild-type or mutant CD86 to identify critical domains for signaling

  • Perform site-directed mutagenesis to determine which CD86 residues are essential for binding CD28 versus CTLA-4

• System-level analysis:

  • Profile transcriptional changes following CD86 engagement using RNA-seq

  • Perform proteomics analysis to identify novel CD86-associated proteins

  • Use computational modeling to integrate CD86 signaling with other costimulatory pathways

These methodological approaches help delineate how CD86 contributes to the "second signal" in T cell activation and how it influences the balance between immunity and tolerance. Understanding these pathways has significant implications for autoimmune disease research and cancer immunotherapy development .

How can I quantitatively assess changes in CD86 expression during cell activation?

For quantitative assessment of CD86 expression changes during activation:

• Flow cytometry-based quantification:

  • Measure both percentage of CD86+ cells and mean fluorescence intensity (MFI)

  • Use quantitative flow cytometry with calibrated beads to determine absolute number of CD86 molecules per cell

  • Track temporal changes in CD86 expression following various activation stimuli

  • Compare CD86 upregulation kinetics across different cell types and activation conditions

• Transcriptional analysis:

  • Perform RT-qPCR to measure CD86 mRNA levels before and after activation

  • Compare protein and mRNA kinetics to understand regulatory mechanisms

  • Use RNA-seq to place CD86 expression changes in the context of global transcriptional programs

• Imaging-based approaches:

  • Use quantitative immunofluorescence microscopy with biotinylated CD86 antibodies

  • Assess changes in subcellular localization and clustering upon activation

  • Perform live-cell imaging to track dynamic changes in CD86 expression and distribution

• Biochemical quantification:

  • Use Western blotting with densitometric analysis

  • Perform ELISA to detect soluble CD86 isoforms

  • Employ surface biotinylation assays to specifically quantify membrane-bound CD86

A comparative study examining CD86 expression on dendritic cells (DCs) found that LPS stimulation significantly enhanced the expression of costimulatory markers including CD86, measured by both mean fluorescence intensity and percentage of positive cells . Interestingly, while biotin deficiency had no significant effect on DC phenotype regarding CD86 expression, it did enhance inflammatory responses, suggesting complex regulation of costimulatory molecule function beyond simple expression levels .

Are there species-specific considerations when using CD86 antibodies across different model organisms?

When working with CD86 antibodies across different species, consider these important factors:

• Antibody selection:

  • Clone IT2.2 monoclonal antibody is specific for human CD86

  • Clone GL1 monoclonal antibody is specific for mouse CD86

  • Polyclonal antibodies may offer broader cross-reactivity (human, mouse, rat, dog, with predicted reactivity to cow, sheep, pig)

• Epitope conservation:

  • Check sequence homology of the target epitope across species

  • The source of the polyclonal antibody (e.g., "derived from rat CD86: 140-175/313") indicates the immunogen region

  • Sequence divergence in this region may affect cross-reactivity

• Expression pattern differences:

  • Mouse CD86 is expressed on activated T cells, while this expression pattern may differ in other species

  • Expression on thioglycolate-elicited peritoneal cells is documented in mice but may vary in other species

  • Activation kinetics may differ between species

• Validation requirements:

  • Always validate antibodies when moving to a new species

  • Include appropriate positive and negative controls specific to each species

  • Consider using multiple antibody clones targeting different epitopes for confirmation

• Application considerations:

  • Flow cytometry protocols may require species-specific optimization

  • Buffer compositions and blocking reagents may need adjustment

  • Secondary detection reagents must be appropriate for the host species of the primary antibody

When planning cross-species studies, the polyclonal antibody (bs-1035R-Biotin) with documented reactivity to human, mouse, rat, and dog may be advantageous for comparative studies, though validation in each species remains essential .

Why am I seeing inconsistent CD86 staining in my flow cytometry experiments?

Inconsistent CD86 staining can result from several methodological and biological factors:

• Technical variables:

  • Antibody concentration: Insufficient titration may result in suboptimal signal-to-noise ratio

  • Incubation conditions: Variations in temperature, time, or buffer composition

  • Cell preparation: Differences in viability, fixation, or permeabilization procedures

  • Instrument settings: Inconsistent voltage settings or improper compensation

  • Streptavidin conjugate variability: Different lots or degradation of fluorophores

• Biological variables:

  • Activation state: CD86 is dynamically regulated and expression levels change rapidly

  • Cell type heterogeneity: Subpopulations may express different levels of CD86

  • Donor variability: Genetic background can influence basal and inducible expression

  • Sample handling: Delayed processing may affect surface protein integrity

• Antibody-specific factors:

  • Lot-to-lot variation: More common with polyclonal antibodies

  • Epitope accessibility: Conformational changes in CD86 may affect antibody binding

  • Competition with ligands: Endogenous CD28 or CTLA-4 may block antibody binding sites

• Protocol optimization strategies:

  • Standardize cell numbers (1-5 × 10^6 cells/mL)

  • Optimize antibody concentration through careful titration

  • Establish consistent gating strategies based on appropriate controls

  • Use calibration beads to normalize MFI values across experiments

  • Include internal standards in each experiment

For technical reproducibility, it's recommended to carefully titrate antibody concentration (≤0.5 μg per test for IT2.2; ≤0.25 μg per test for GL1) and maintain consistent experimental conditions across studies .

How can I distinguish between genuine CD86 expression and background signal?

To differentiate between true CD86 expression and background signal:

• Control implementation:

  • Use isotype controls matched to the primary antibody's host species and immunoglobulin class

  • Include fluorescence minus one (FMO) controls in multicolor panels

  • Compare with known negative cell populations

  • Use CD86-blocking approaches as functional controls

• Titration optimization:

  • Perform antibody titration experiments to identify the concentration that maximizes the signal-to-noise ratio

  • Plot signal-to-noise ratio versus antibody concentration to identify optimal staining conditions

  • Recommended starting points: ≤0.5 μg per test for IT2.2 (human); ≤0.25 μg per test for GL1 (mouse)

• Analytical approaches:

  • Use biexponential display scales to visualize both dim and bright populations

  • Apply consistent gating strategies based on controls

  • Consider statistical approaches such as Overton subtraction or probability binning

  • Examine both percentage positive and MFI values

• Validation strategies:

  • Confirm expression using antibodies targeting different CD86 epitopes

  • Correlate protein detection with mRNA expression

  • Use biological stimulation (LPS, CD40L) to confirm expected upregulation patterns

A study examining CD86 expression on dendritic cells demonstrated that while biotin deficiency did not affect CD86 expression levels, LPS stimulation significantly upregulated CD86 expression, providing a useful positive control for distinguishing genuine expression from background . This approach of comparing resting and activated cells can be particularly valuable for validating CD86 detection methods.

What factors might affect CD86 antibody binding efficiency?

Multiple factors can influence CD86 antibody binding efficiency:

• Sample preparation factors:

  • Cell viability: Dead or dying cells often show increased non-specific binding

  • Fixation effects: Some fixatives may mask or alter CD86 epitopes

  • Buffer composition: Presence of divalent cations, pH, and protein content

  • Fc receptor blocking: Insufficient blocking can increase background

• Antibody characteristics:

  • Epitope accessibility: Conformational changes in CD86 may affect binding

  • Clone-specific properties: Different affinity and avidity between clones (IT2.2, GL1)

  • Biotin:antibody ratio: Over-biotinylation can decrease antibody activity

  • Storage conditions: Freeze-thaw cycles and improper storage temperature

• Biological variables:

  • Ligand occupancy: Endogenous CD28/CTLA-4 binding may block antibody access

  • Glycosylation patterns: Variable glycosylation can affect epitope recognition

  • Isoform expression: Alternative splicing creates multiple CD86 isoforms

  • Internalization kinetics: CD86 receptor cycling can affect surface availability

• Technical considerations:

  • Incubation temperature: Cold (2-8°C) versus room temperature protocols

  • Incubation time: Insufficient or excessive incubation

  • Washing procedures: Incomplete washing can increase background

  • Streptavidin conjugate quality: Degraded fluorophores reduce signal intensity

To optimize binding efficiency, maintain proper storage conditions for antibodies (store at -20°C as recommended), include appropriate Fc blocking steps, optimize incubation conditions, and ensure filtration quality (0.2 μm post-manufacturing filtered antibodies are recommended) .

How should I interpret CD86 expression data in the context of immune activation?

When interpreting CD86 expression data in the context of immune activation:

• Expression level considerations:

  • Baseline expression: Low levels on resting B cells, macrophages, and dendritic cells

  • Activation markers: Compare CD86 upregulation with other activation markers (CD80, HLA-DR)

  • Kinetics: CD86 is typically upregulated rapidly upon activation, supporting its major contribution during the primary phase of immune responses

  • Cell-type specific patterns: Different APC types show distinct CD86 expression dynamics

• Functional correlations:

  • T cell responses: Correlate CD86 levels with T cell proliferation and cytokine production

  • Costimulatory balance: Examine the ratio of CD86 to other costimulatory/inhibitory molecules

  • Threshold effects: Determine minimum CD86 expression required for effective T cell activation

  • Regulation mechanisms: Analyze how CD86 expression relates to tolerance versus activation

• Analytical frameworks:

  • Percentage positive vs. MFI: Analyze both metrics as they provide complementary information

  • Bimodal distributions: Investigate whether discrete CD86-high and CD86-low populations exist

  • Population heterogeneity: Correlate CD86 expression with other phenotypic markers

  • Temporal dynamics: Track expression changes over time following stimulation

• Experimental context:

  • Stimulation conditions: Different stimuli (BCR engagement, CD40 ligation, cytokines) induce distinct CD86 expression patterns

  • Species differences: Human and mouse cells may show different expression dynamics

  • In vitro vs. in vivo: Consider how culture conditions may affect expression compared to physiological settings

How is CD86 expression altered in inflammatory conditions?

CD86 expression undergoes significant changes during inflammatory responses:

• Acute inflammation:

  • Rapid upregulation on antigen-presenting cells following exposure to:

    • Pathogen-associated molecular patterns (PAMPs)

    • Damage-associated molecular patterns (DAMPs)

    • Pro-inflammatory cytokines

  • Enhanced CD86 expression correlates with increased T cell activation capacity

  • Changes may occur in both percentage of CD86+ cells and expression intensity (MFI)

• Chronic inflammation:

  • Persistently elevated CD86 levels on tissue-resident APCs

  • Altered ratio of CD86 to inhibitory molecules

  • Changes in CD86 isoform distribution

  • Modification of downstream signaling pathways

• Tissue-specific patterns:

  • Mucosal surfaces: Distinct regulation compared to peripheral blood

  • Central nervous system: Microglia upregulate CD86 during neuroinflammation

  • Synovial tissue: Elevated CD86 in rheumatoid arthritis

  • Skin: Increased CD86+ dendritic cells in psoriasis and dermatitis

• Methodological approaches:

  • Flow cytometry of cells from inflamed tissues

  • Immunohistochemistry using biotinylated antibodies with streptavidin-HRP

  • Single-cell RNA sequencing to correlate CD86 with inflammatory gene programs

  • In vivo models using CD86 reporter systems

A study examining dendritic cells found that LPS stimulation significantly enhanced the expression of costimulatory markers including CD86, confirming its role as an inflammatory marker . This upregulation represents a critical step in APC maturation that enables effective T cell activation during inflammatory responses. Interestingly, while biotin deficiency enhanced inflammatory responses of dendritic cells, it did not significantly affect CD86 expression levels, suggesting complex regulation of inflammation beyond costimulatory molecule expression .

What role does CD86 play in cancer immunotherapy research?

CD86 has emerged as a significant factor in cancer immunotherapy research:

• Tumor microenvironment interactions:

  • Reduced CD86 expression on tumor-associated APCs contributes to immunosuppression

  • Tumor cells may downregulate CD86 on infiltrating dendritic cells

  • CD86 expression correlates with T cell infiltration and activation status

  • Ratio of CD86 to inhibitory molecules (PD-L1) may predict immunotherapy responsiveness

• Therapeutic targeting strategies:

  • Enhancing CD86 expression on APCs to improve anti-tumor immunity

  • Engineering CAR-T cells to deliver CD86 costimulatory signals

  • Combining CD86 agonism with checkpoint inhibitor therapies

  • Developing CD86-targeted imaging approaches for monitoring immune responses

• Research applications:

  • Flow cytometric analysis of CD86 on tumor-infiltrating APCs

  • Tissue microarray analysis using biotinylated CD86 antibodies

  • Correlation of CD86 expression with clinical outcomes

  • Functional studies of T cell activation in the presence of CD86-expressing versus CD86-deficient APCs

• Biomarker potential:

  • CD86 expression on circulating monocytes as a predictive biomarker

  • Changes in CD86 levels during immunotherapy as pharmacodynamic markers

  • Soluble CD86 in patient serum as a prognostic indicator

  • CD86 polymorphisms as predictors of therapy response

Specific malignancies such as gallbladder squamous cell carcinoma have been associated with CD86 dysfunction, highlighting its relevance in cancer biology . Research on CD86 in the cancer context is facilitated by antibodies that enable precise detection and quantification in both flow cytometry and tissue-based applications .

How can CD86 antibodies help study immune tolerance mechanisms?

Biotinylated CD86 antibodies serve as valuable tools for investigating immune tolerance:

• Tolerance induction mechanisms:

  • Antigen presentation without sufficient CD86/CD80 costimulation can induce tolerance

  • CD86 detection helps identify APCs with tolerogenic versus immunogenic phenotypes

  • Flow cytometric analysis can correlate CD86 expression with regulatory T cell induction

  • Imaging studies can visualize CD86 distribution during tolerogenic APC-T cell interactions

• Self-tolerance maintenance:

  • Examine CD86 expression on APCs in peripheral tolerance models

  • Investigate how regulatory T cells modulate CD86 expression on APCs

  • Study CD86 in thymic selection processes

  • Compare CD86 levels in steady-state versus inflammatory conditions

• Therapeutic tolerance induction:

  • Track CD86 expression during tolerogenic therapies

  • Monitor changes in CD86:inhibitory molecule ratios

  • Assess how tolerogenic protocols affect CD86 expression kinetics

  • Correlate CD86 levels with functional tolerance outcomes

• Methodological approaches:

  • Flow cytometry with biotinylated CD86 antibodies to quantify expression

  • Functional assays comparing wild-type and CD86-blocked APCs

  • In vivo imaging of CD86+ cells during tolerance induction

  • Single-cell analysis correlating CD86 with tolerogenic transcriptional programs

The critical role of CD86 in determining tolerance versus immunity is highlighted by the finding that antigen presentation without sufficient CD86/CD80 costimulation leads to tolerance rather than activation . This principle underlies therapeutic approaches that modulate CD86 signaling to induce tolerance in autoimmunity and transplantation. Biotinylated CD86 antibodies enable detailed characterization of APC phenotypes during these processes, providing crucial insights into tolerance mechanisms .

What is known about CD86 dysfunction in specific disease states?

CD86 dysfunction has been implicated in several disease processes:

• Gallbladder squamous cell carcinoma:

  • Altered CD86 expression patterns in tumor tissue

  • Impaired costimulatory function affecting anti-tumor immunity

  • Potential prognostic significance of CD86 expression levels

  • Molecular mechanisms involving dysregulated CD86 signaling pathways

• Myocarditis:

  • Abnormal CD86 expression on cardiac-infiltrating APCs

  • Imbalanced costimulatory signals contributing to pathological T cell responses

  • Potential therapeutic target for modulating cardiac inflammation

  • Correlation between CD86+ cell density and disease severity

• Autoimmune disorders:

  • Enhanced CD86 expression on APCs in active disease phases

  • Polymorphisms in CD86 associated with disease susceptibility

  • Altered CD86 glycosylation affecting binding properties

  • Therapeutic targeting of CD86-CD28 interactions

• Infectious diseases:

  • Pathogen-mediated manipulation of CD86 expression

  • Changes in CD86 isoform distribution during chronic infection

  • Correlation between CD86 levels and protective versus pathological immunity

  • Species-specific differences in infection-induced CD86 regulation

• Methodological approaches:

  • Immunohistochemistry using biotinylated CD86 antibodies on disease tissues

  • Flow cytometric analysis of CD86 on patient-derived cells

  • Genetic association studies examining CD86 polymorphisms

  • Animal models with CD86 deficiency or overexpression

Research has identified gallbladder squamous cell carcinoma and myocarditis as specific conditions associated with CD86 dysfunction . These findings highlight the importance of proper CD86 signaling in maintaining immune homeostasis and suggest potential therapeutic avenues targeting this pathway. The availability of various biotinylated CD86 antibodies with different species reactivity profiles facilitates comparative studies across disease models .