CD86 Antibody, FITC

What is CD86 and why is it important in immunological research?

CD86 (also known as B7-2) is a type I transmembrane protein belonging to the immunoglobulin superfamily that functions as a critical costimulatory molecule in immune responses. It is one of two ligands (along with CD80) for CD28 and CTLA-4 receptors on T cells . CD86 is predominantly expressed on antigen-presenting cells, including dendritic cells, activated B cells, and monocytes/macrophages .

The significance of CD86 in research stems from its fundamental role in T cell activation. When CD86 binds to CD28, it provides a costimulatory signal essential for T cell proliferation and interleukin-2 production . Conversely, binding to CTLA-4 delivers an inhibitory signal that regulates T cell activation and diminishes immune responses . This dual functionality makes CD86 central to understanding immune regulation and tolerance.

Research has demonstrated that CD86 is expressed earlier in immune responses than CD80, suggesting distinct temporal roles in immune regulation . Additionally, CD86 is involved in immunoglobulin class-switching and triggering NK cell-mediated cytotoxicity, highlighting its diverse functions beyond T cell costimulation .

How do FITC-conjugated CD86 antibodies function in flow cytometry applications?

FITC-conjugated CD86 antibodies combine specific recognition of CD86 molecules with fluorescent detection capabilities for flow cytometric analysis. The antibody portion binds specifically to CD86 expressed on cell surfaces, while the FITC (Fluorescein isothiocyanate) fluorophore enables detection when excited by a blue laser (488 nm) .

The technical aspects of FITC-conjugated antibodies include:

• Excitation at 488 nm with emission detected using optical filters centered near 530 nm (typically a 525/40 nm bandpass filter)

• Relatively high absorptivity and excellent fluorescence quantum yield

• Good water solubility, enhancing staining performance in aqueous buffers

• Optimization for blue laser detection on standard flow cytometers

For optimal results, researchers typically use 5-10 μL of antibody per test (defined as the amount required to stain approximately 10^6 cells in 100 μL volume) . The fluorescence intensity correlates with the level of CD86 expression, allowing for quantitative assessment of this costimulatory molecule across different cell populations and activation states.

What cell types express CD86 and how does expression change during immune activation?

CD86 expression varies considerably across immune cell types and is dynamically regulated during immune responses:

Expression Pattern by Cell Type:

• Dendritic cells: Express intermediate to high levels, particularly upon maturation

• B cells: Germinal center B cells constitutively express CD86; resting B cells show minimal expression

• Monocytes/macrophages: Express low to intermediate levels, increasing upon activation

• Eosinophils: CD86 expression documented in allergic conditions

• Non-lymphoid cells: Some expression detected in thymic cells

Dynamic Regulation During Immune Responses:

• Resting B cells express minimal CD86, but rapidly upregulate expression following activation with stimuli like LPS

• CD86 is typically expressed earlier in immune responses than CD80

• The kinetics of CD86 upregulation support its major contribution during the primary phase of immune responses

• CD86 is constitutively expressed in naive murine lung tissue and can be found on eosinophils in allergic lung, suggesting tissue-specific regulation relevant to respiratory immunity

Research indicates that CD86 expression can be rapidly induced within hours of appropriate stimulation, making it an early marker of cellular activation and a critical component of the initial immune response to antigens .

What are the functional differences between CD86 (B7-2) and CD80 (B7-1)?

Although CD86 (B7-2) and CD80 (B7-1) are both B7 family costimulatory molecules that bind to CD28 and CTLA-4, they exhibit several important functional and expression differences:

Research on murine models of allergic airway inflammation has demonstrated that signaling through either CD80 or CD86 is sufficient to generate a partial local allergic response, whereas CD86 costimulation is specifically essential for inducing systemic allergic (IgE) reactions . This suggests that CD86 has a more critical role in certain types of immune responses, particularly those involving humoral immunity.

Combined anti-CD80/anti-CD86 treatment fully blocks the development of allergic airways inflammation, whereas partial reduction is observed in mice treated with either anti-CD80 or anti-CD86 antibody alone . This highlights the complementary yet partially non-redundant functions of these two costimulatory molecules.

What are the optimal staining conditions for FITC-conjugated anti-CD86 antibodies?

Achieving optimal staining with FITC-conjugated anti-CD86 antibodies requires careful attention to sample preparation, antibody concentration, and staining conditions:

Sample Preparation:

• Maintain cell viability above 90% for reliable results

• Use freshly isolated cells whenever possible

• Keep cells at 4°C during staining to prevent internalization of surface markers

• For peripheral blood, isolate mononuclear cells using density gradient centrifugation

Antibody Concentration and Staining Protocol:

• For most applications, use 5-10 μL of antibody per test (approximately 10^6 cells in 100 μL)

• For clones like BU63, the manufacturer typically recommends ≤0.5 μg per test

• Incubate cells with antibody for 20-30 minutes at 4°C in the dark

• Wash cells twice with cold PBS containing 1-2% protein (BSA or FBS)

• If analysis is delayed, fix cells with 1-2% paraformaldehyde

Buffer Considerations and Technical Precautions:

• Use staining buffer containing protein (BSA or FBS) to reduce non-specific binding

• Protect samples from light throughout the procedure to prevent FITC photobleaching

• Store the antibody at 2-8°C and avoid freeze-thaw cycles that can damage the reagent

• For optimal performance, use the antibody within the manufacturer's recommended shelf life (typically 12 months)

Titration of the antibody is crucial for optimal signal-to-noise ratio and should be determined empirically for each specific application and cell type . Different cell types may require adjustment of antibody concentration for optimal staining.

How should I design a flow cytometry panel that includes CD86-FITC?

Designing an effective flow cytometry panel incorporating CD86-FITC requires careful consideration of spectral compatibility, marker expression levels, and research objectives:

Spectral Considerations:

• FITC is excited by the 488 nm blue laser and emits at approximately 520 nm

• Consider potential spectral overlap with other fluorochromes, particularly PE

• Plan appropriate compensation controls if using multiple fluorochromes

• FITC has moderate brightness—consider this when designing panels for detecting low-expression antigens

Panel Design Principles:

• Allocate brightest fluorochromes to least expressed markers and vice versa

• Assign markers expected on the same cell to fluorochromes with minimal spillover

• Include CD86-FITC alongside complementary markers based on research questions:

Example Panels for Common Research Applications:

When establishing the panel, validate the staining performance of each antibody individually before combining them, and ensure proper compensation settings to address spectral overlap issues that could compromise data quality .

What controls are essential when using CD86-FITC antibodies?

When conducting experiments with CD86-FITC antibodies, several controls are essential to ensure valid and interpretable results:

Fundamental Controls:

• Unstained control: Cells without any antibody to establish autofluorescence baseline

• Isotype control: FITC-conjugated mouse IgG1, κ (matching the antibody's isotype) to assess non-specific binding

  • For BU63 clone, the appropriate isotype control is Mouse IgG1, κ (e.g., E-AB-F09792C)

  • For 24F clone, a matching mouse IgG isotype should be used

• Single-color controls: Required for each fluorochrome in multicolor panels to calculate compensation

• FMO (Fluorescence Minus One): All antibodies in your panel except CD86-FITC to establish proper gating boundaries

Biological Controls:

• Negative cell population: Cells known not to express CD86 (e.g., resting T cells)

• Positive cell population: Cells known to express CD86 (e.g., LPS-activated B cells, mature dendritic cells)

• Stimulation control: Compare unstimulated vs. stimulated cells (e.g., with LPS) to confirm biological response

• Blocking control: Pre-incubation with unconjugated anti-CD86 to verify staining specificity

Technical Validation:

• Titration control: Test different antibody concentrations to determine optimal staining

• Viability discrimination: Include a viability dye to exclude dead cells that can bind antibodies non-specifically

• Time-course control: If studying activation dynamics, include multiple time points to capture expression kinetics

These controls are critical for discriminating true CD86 expression from artifacts and for proper interpretation of experimental results, particularly when studying cells with variable or low CD86 expression levels .

How does CD86 expression differ between resting and activated immune cells?

CD86 expression is dramatically regulated during immune cell activation, with distinct patterns across different cell types:

B Cells:

• Resting B cells express minimal CD86 on their surface

• Upon activation (e.g., with LPS, CD40L, or BCR engagement), B cells rapidly upregulate CD86 within 4-6 hours

• Germinal center B cells constitutively express higher levels of CD86 compared to naive B cells

• Flow cytometric analysis typically shows a 5-10 fold increase in CD86 mean fluorescence intensity following activation

Dendritic Cells:

• Immature DCs express moderate levels of CD86

• Upon exposure to maturation stimuli (PAMPs, inflammatory cytokines), DCs significantly upregulate CD86

• Mature DCs exhibit high, stable CD86 expression that contributes to their potent T cell stimulatory capacity

• The CD86:CD80 expression ratio changes during DC maturation, with CD86 typically induced earlier

Monocytes/Macrophages:

• Resting monocytes express low levels of CD86

• Upon activation, monocytes increase CD86 expression within hours

• Macrophage polarization affects CD86 expression patterns (M1 vs. M2)

• Tissue-resident macrophages show tissue-specific regulation of CD86

Quantitative Assessment:
Research has demonstrated that the kinetics of CD86 upregulation support its major contribution during the primary phase of immune responses . This temporal advantage of CD86 over CD80 (which is typically expressed later) highlights its importance in initiating adaptive immune responses.

The differential regulation of CD86 across cell types and activation states makes it an excellent marker for monitoring immune cell activation in various experimental settings and disease contexts .

Why might I observe variable CD86 expression levels across samples?

Variability in CD86 expression across samples can stem from multiple biological and technical factors:

Biological Sources of Variation:

• Activation status: CD86 is rapidly upregulated upon cell activation; minor differences in activation state can significantly impact expression levels

• Cell subpopulation distribution: Different antigen-presenting cell subsets express varying levels of CD86

• Donor variability: Genetic factors and underlying immune status can influence basal and inducible CD86 expression

• Temporal dynamics: CD86 expression changes rapidly over the course of immune responses, with earlier expression than CD80

• Disease status: Inflammatory or allergic conditions may alter CD86 expression patterns

Technical Factors:

• Sample handling: Delays between collection and processing can activate cells and alter CD86 expression

• Antibody clone differences: Different anti-CD86 clones (e.g., BU63 vs. 24F) may have different binding characteristics

• Staining protocol variations: Temperature, incubation time, and buffer composition affect staining efficiency

• Instrument settings: Inconsistent cytometer settings between experiments lead to apparent variations

• FITC susceptibility: FITC is sensitive to photobleaching and pH changes, potentially affecting staining intensity

Methodological Solutions:

• Implement standardized protocols for sample collection, processing, and staining

• Include reference controls in each experiment

• Document and control for the activation status of cells

• Consider using quantitative beads to normalize fluorescence intensity across experiments

• For longitudinal studies, freeze aliquots of control cells for consistent comparison

Understanding the dynamic nature of CD86 expression is crucial for interpreting experimental results, particularly when studying temporal aspects of immune activation or comparing different donor samples .

How can I distinguish true CD86 signal from autofluorescence?

Distinguishing genuine CD86-FITC signal from autofluorescence is crucial for accurate data interpretation, especially when studying cells with naturally high autofluorescence:

Methodological Approaches:

• Control implementation: Always include unstained controls and isotype controls matched to your anti-CD86 antibody (Mouse IgG1, κ for BU63 clone)

• FMO (Fluorescence Minus One): Include all antibodies except CD86-FITC to establish accurate gating boundaries

• Viability discrimination: Dead cells often exhibit increased autofluorescence; exclude using appropriate viability dyes

• Spectral unmixing: Apply computational approaches to separate FITC signal from autofluorescence spectra

Technical Optimization:

• Voltage settings: Optimize PMT voltages to maximally separate positive and negative populations

• Compensation: Properly compensate for spectral overlap from other fluorochromes

• Filter selection: Ensure the optical filter configuration optimally captures FITC emission (525/40 nm bandpass filter)

• Alternative approaches: For highly autofluorescent samples, consider:

  • Using brighter fluorochromes (PE, APC) for CD86 detection

  • Autofluorescence reduction through quenching reagents

  • Alternative stimulation protocols that minimize autofluorescence

Analysis Strategies:

• Biexponential display: Use biexponential scaling to better visualize the full range of fluorescence

• Population comparison: Compare CD86 expression between populations known to be positive versus negative

• Stimulation assessment: Compare CD86 expression before and after known stimulation (e.g., LPS) to confirm biological response

• Blocking validation: Pre-block with unconjugated anti-CD86 to confirm specificity of FITC signal

According to the technical specifications, FITC is designed to be excited by the blue laser (488 nm) and detected using a 525/40 nm bandpass filter . Optimizing your instrument for this specific detection range will help differentiate true signal from autofluorescence.

What might cause reduced staining efficiency with CD86-FITC antibodies?

Several factors can contribute to suboptimal staining with CD86-FITC antibodies:

Sample-Related Issues:

• Cell viability: Dead or dying cells may exhibit altered epitope expression or non-specific binding

• Receptor internalization: Activation can cause CD86 internalization, reducing surface detection

• Epitope masking: Binding of endogenous ligands (CD28/CTLA-4) may block antibody access

• Enzymatic degradation: Proteolytic enzymes in sample preparation may damage CD86 epitopes

Antibody-Related Factors:

• Photobleaching: FITC is particularly susceptible to photobleaching; exposure to light degrades signal

• Antibody degradation: Improper storage or freeze-thaw cycles can damage antibody structure

• Concentration issues: Incorrect antibody titration leads to weak staining or high background

• Clone specificity: Different anti-CD86 clones (BU63, 24F) recognize different epitopes with varying affinities

Technical Considerations:

• Buffer incompatibility: Certain buffers may interfere with antibody binding or FITC fluorescence

• Incubation conditions: Suboptimal temperature or duration affects binding efficiency

• Washing procedures: Excessive washing removes bound antibody; insufficient washing leaves background

• Instrument settings: Improper cytometer configuration reduces sensitivity for FITC detection

Solutions and Best Practices:

• Store antibodies according to manufacturer recommendations (typically 2-8°C, protected from light)

• Prepare fresh antibody dilutions for critical experiments

• Titrate antibody to determine optimal concentration for your specific cell type

• Include positive control samples to verify antibody performance

• Protect samples from light during all stages of staining and analysis

• Optimize staining buffers to include protein (BSA/FBS) for stabilization

According to manufacturer information, FITC-conjugated anti-CD86 antibodies should be stored at 2-8°C for up to 12 months and protected from prolonged light exposure . Following these recommendations will help maintain optimal antibody performance and staining efficiency.

How do I properly interpret CD86/CD80 co-expression data?

Interpreting CD86/CD80 co-expression requires consideration of their complementary yet distinct roles in immune regulation:

Analytical Framework:

• Quadrant analysis: Plot CD86 versus CD80 expression to identify single-positive, double-positive, and double-negative populations

• Temporal considerations: CD86 is typically expressed earlier than CD80 during immune responses

• Relative expression analysis: The ratio of CD86:CD80 may be more informative than absolute levels

• Functional correlation: Connect expression patterns with functional readouts (T cell proliferation, cytokine production)

Biological Interpretation of Expression Patterns:

• CD86+/CD80- cells: Typically represent early-activated or partially mature APCs

• CD86+/CD80+ cells: Often indicate fully mature or strongly activated APCs

• CD86-/CD80+ cells: Less common, may represent cells in later stages of activation

• Expression dynamics: Shifts in CD86:CD80 ratio during responses reflect changing costimulatory environment

Research Context-Specific Interpretation:

• Tolerance induction: Antigen presentation with insufficient CD86/CD80 costimulation can induce tolerance

• T helper differentiation: CD86 appears to play a role distinct from CD80 in T helper cell differentiation

• Systemic versus local responses: Research indicates that signaling through either CD80 or CD86 can generate partial local allergic responses, whereas CD86 costimulation is specifically essential for systemic allergic (IgE) reactions

Technical Considerations:

• Ensure proper compensation between fluorochromes used for CD86 and CD80

• Include FMO controls for accurate gating of both markers

• Consider using dimensional reduction techniques (tSNE, UMAP) for complex datasets

• Validate flow cytometry findings with complementary techniques (immunofluorescence, functional assays)

Research demonstrates that combined anti-CD80/anti-CD86 treatment blocks allergic airway responses more effectively than either antibody alone, highlighting their complementary yet partially redundant functions . This should be considered when interpreting co-expression patterns in both basic research and therapeutic contexts.

How can CD86-FITC antibodies be used to study T cell costimulation in vitro?

CD86-FITC antibodies provide powerful tools for investigating T cell costimulation mechanisms through several sophisticated experimental approaches:

Experimental Models:

• Mixed lymphocyte reactions (MLR): Track CD86 expression on APCs during allogeneic T cell responses

• T cell/APC co-culture systems: Monitor CD86 expression changes during antigen presentation

• Time-course activation analysis: Study temporal patterns of CD86 upregulation following various stimuli

• Blocking experiments: Use unconjugated anti-CD86 alongside CD86-FITC to assess functional outcomes

Advanced Methodological Approaches:

• FACS-based cell sorting: Isolate CD86high versus CD86low APCs to test differential stimulatory capacity

• Imaging flow cytometry: Visualize CD86 clustering and immunological synapse formation

• Real-time analysis: Track CD86 expression kinetics on live cells during T cell interactions

• Multi-parameter analysis: Combine CD86-FITC with markers for T cell activation (CD25, CD69) and cytokine production

Mechanistic Investigation Protocol:

• Isolate APCs (dendritic cells or B cells) and purify T cells from appropriate sources

• Expose APCs to various stimuli (LPS, CD40L, cytokines) to induce CD86 expression

• Quantify CD86 upregulation using CD86-FITC antibody via flow cytometry

• Co-culture stimulated APCs with T cells at different ratios

• Assess T cell activation markers, proliferation (CFSE dilution), and cytokine production

• Perform blocking experiments with anti-CD86 antibodies or CTLA4-Ig

• Correlate CD86 expression levels with functional T cell outcomes

Data Analysis Considerations:

• Quantify both percentage of CD86+ cells and mean fluorescence intensity

• Establish dose-response relationships between CD86 expression and T cell activation

• Analyze kinetic data to determine optimal timing for costimulatory interactions

• Compare CD86 contribution relative to other costimulatory pathways

According to research findings, CD86 binding to CD28 transduces costimulatory signals for T cell activation, proliferation, and cytokine production, while binding to CTLA-4 delivers inhibitory signals . This dual functionality makes CD86-FITC antibodies valuable tools for dissecting the complex regulation of T cell responses in various experimental models.

What are the best approaches to study CD86/CD28 interactions in disease models?

Studying CD86/CD28 interactions in disease models requires integrated approaches combining molecular, cellular, and in vivo techniques:

In Vivo Model Systems:

• Genetic approaches:

  • CD86 knockout or conditional knockout mice

  • CD86 reporter mice for real-time expression monitoring

  • Cell-specific CD86 deletion to identify crucial cellular sources

• Antibody-mediated interventions:

  • Anti-CD86 blocking antibodies administered at different disease stages

  • Comparison of anti-CD86 versus anti-CD80 versus combined blockade

  • Timing experiments to determine critical windows for intervention

• Disease-specific models:

  • Allergic airway inflammation models (demonstrate CD86's role in IgE production)

  • Autoimmune models (EAE, collagen-induced arthritis)

  • Transplantation models (allograft rejection, GVHD)

  • Tumor immunology models (anti-tumor immunity)

Analytical Approaches:

• Flow cytometry applications:

  • Multi-parameter analysis of CD86 across immune cell subsets during disease progression

  • Correlation of CD86 expression with disease markers and clinical outcomes

  • Ex vivo restimulation to assess functional capacity

• Imaging methods:

  • Intravital microscopy to visualize CD86/CD28 interactions in living tissue

  • Immunohistochemistry to map CD86 expression within diseased tissue architecture

  • Proximity ligation assays to detect actual CD86/CD28 binding events

• Molecular analyses:

  • Transcriptomic profiling to identify programs associated with CD86 signaling

  • Single-cell approaches to resolve heterogeneity in CD86 expression and response

Experimental Design Considerations:

• Include both prevention (pre-disease) and treatment (established disease) protocols

• Assess both local and systemic immune parameters

• Combine blocking studies with expression analysis using CD86-FITC antibodies

• Include functional readouts relevant to the specific disease model

Research on murine models of allergic airway inflammation demonstrates that CD86 plays a particularly important role in systemic manifestations of allergy, as anti-CD86 specifically blocks systemic IgE production . Additionally, combined anti-B7 monoclonal antibody treatment after sensitization reduces airway eosinophilia and cytokine secretion, confirming CD86's ongoing role in the effector phase of disease . These findings highlight the importance of studying both local and systemic aspects of CD86 function in disease models.

How does blocking CD86 with antibodies affect experimental outcomes in immunology?

Blocking CD86 with antibodies can profoundly impact experimental outcomes in immunology, with effects that vary depending on context, timing, and whether CD80 is simultaneously blocked:

Immunological Effects:

• T cell responses:

  • Reduced T cell proliferation and IL-2 production in response to antigen

  • Altered Th1/Th2 balance (often reducing Th2-type responses)

  • Impaired development of T cell memory

  • Potential enhancement of regulatory T cell function

• B cell responses:

  • Decreased antibody production, particularly affecting certain isotypes

  • Specific blockade of systemic IgE production in allergic models

  • Altered immunoglobulin class switching

  • Impaired germinal center formation

• Regulatory mechanisms:

  • Induction of T cell anergy or tolerance under specific conditions

  • Modified balance between activating (CD28) and inhibitory (CTLA-4) signals

Model-Specific Outcomes:

• Allergic inflammation:

  • Anti-CD86 treatment reduces airway eosinophilia and IL-4/IL-5 cytokine secretion

  • Specifically blocks systemic IgE production while maintaining partial local inflammation

  • Most effective when administered during both sensitization and challenge phases

  • Combined anti-CD80/CD86 treatment provides more complete protection than either alone

• Autoimmunity models:

  • Ameliorates disease severity in multiple sclerosis and arthritis models

  • Most effective when administered early in disease development

  • Often requires combination with other immunomodulatory approaches for maximal effect

• Transplantation models:

  • Prolongs allograft survival

  • Can promote tolerance induction under specific conditions

  • Efficacy depends on timing and combination with other immunosuppressive strategies

Technical and Experimental Considerations:

• Different anti-CD86 antibody clones may have varying blocking efficacy

• Dose-dependent effects: Partial versus complete blockade yields different outcomes

• Timing is critical: Effects differ in prevention versus treatment protocols

• Species differences must be considered when translating findings from animal models

Research demonstrates that combined anti-B7 monoclonal antibody treatment after sensitization reduces airway eosinophilia and IL-4/IL-5 cytokine secretion, confirming CD86's ongoing role in the effector phase of allergic disease . This highlights the potential therapeutic value of targeting CD86 not only for prevention but also for treatment of established immune-mediated conditions.

What role does CD86 play in different autoimmune and inflammatory conditions?

CD86 contributes significantly to the pathogenesis of various autoimmune and inflammatory conditions, though its precise role varies depending on the specific disease context:

Respiratory Disorders:

• Allergic asthma and airway inflammation:

  • CD86 is constitutively expressed in naive murine lung and on eosinophils in allergic lung

  • CD86 costimulation is essential for systemic IgE production in allergic responses

  • CD86 blockade reduces airway eosinophilia and Th2 cytokine production (IL-4/IL-5)

  • Critical for both sensitization and effector phases of allergic airway disease

• Chronic respiratory conditions:

  • Altered CD86 expression on alveolar macrophages correlates with disease severity

  • CD86+ dendritic cells contribute to pathogenic T cell activation in lung tissue

  • Differential expression between acute and chronic inflammatory states

Systemic Autoimmune Diseases:

• Rheumatoid arthritis:

  • Elevated CD86 expression on APCs in synovial tissue

  • CD86 blockade reduces inflammatory cytokine production in experimental models

  • Potential therapeutic target, particularly in early disease stages

• Multiple sclerosis and experimental autoimmune encephalomyelitis (EAE):

  • CD86 expression on microglia contributes to central nervous system inflammation

  • Temporal dynamics of CD86 expression correlate with disease phases

  • CD28/B7 pathway blockade can ameliorate disease progression

Therapeutic Implications:

• CD86 serves as a biomarker for inflammatory activity in several conditions

• Targeting CD86 provides therapeutic benefit through multiple mechanisms

• Combined approaches blocking both CD80 and CD86 often show superior efficacy

• Timing of intervention is critical for optimal therapeutic outcomes

• CD86-targeted approaches may allow more selective modulation than broader immunosuppression

Research findings demonstrate that the CD28/B7 costimulatory pathway plays an ongoing role in the effector phase of allergic disease, as anti-B7 monoclonal antibody treatment after sensitization reduced airway eosinophilia and pathogenic cytokine secretion . Additionally, CD86 appears particularly important for systemic manifestations of immune-mediated diseases, as evidence from allergic models shows that only anti-CD86 (not anti-CD80) blocked systemic IgE production . These results emphasize the importance of differential B7 expression patterns in various tissues and disease contexts.