Anti-CD36 antibodies are implicated in:
FNAIT and foetal anaemia: CD36-negative mothers develop alloantibodies against CD36-positive fetal erythroid progenitors, leading to severe anaemia .
Immune thrombocytopenia: Alloantibodies cause platelet destruction, contributing to transfusion refractoriness .
Transfusion-related acute lung injury (TRALI): Anti-CD36 antibodies in donor plasma may trigger lung injury .
Recent studies highlight improved diagnostic methods:
Monoclonal antibodies (mAbs) like GZ-70 and GZ-608 outperform traditional mAbs (e.g., FA6-152) in detecting anti-CD36 antibodies. For example:
Clone 5-271: Conjugated with APC for flow cytometry, enabling precise platelet/monocyte analysis .
IHC applications: CD36 antibodies (e.g., 185-1G2) localize to macrophages, adipocytes, and endothelial cells .
CD36 meets criteria for a new blood group system:
Polymorphism: CD36-negative phenotype (rs146027667:T allele) with global minor allele frequency of 0.1% .
Hemolysis risk: Anti-CD36 causes fetal anaemia and neonatal thrombocytopenia .
Inheritance: Autosomal codominant trait, validated in family studies .
Transfusion Medicine: CD36 typing prevents alloimmune complications in platelet/RBC transfusions.
Therapeutic Monitoring: Anti-CD36 antibody levels predict disease outcomes in FNAIT and TRALI .
Basic Research: CD36 serves as a marker for erythroid progenitors (e.g., BFU-E/CFU-E) .
STRING: 6239.C27H5.5
UniGene: Cel.15771
FAQs for Researchers on IL-36/CD36 Antibodies in Academic Research
IL-36 and CD36 antibodies are critical tools in studying immune signaling, tumorigenesis, and metabolic regulation. Below are FAQs addressing key research challenges and methodologies, categorized into basic and advanced questions.
In vitro assays:
In vivo models:
Flow cytometry: Use clones like FA6.152 (anti-CD36) to identify CD36+ cells (monocytes, platelets, erythroid precursors) in human or murine samples .
Functional assays: Test CD36’s role in fatty acid uptake or thrombospondin binding using knockout models or blocking antibodies .
Key findings:
IL-36 agonists induce chemokines linked to tumor progression (e.g., CXCL-1, TGFβ), enhancing migration, angiogenesis, and stromal recruitment .
| Chemokine | Role in CRC | Induction by IL-36 |
|---|---|---|
| CXCL-1 | Adenoma-adenocarcinoma transition, angiogenesis | Strong (human/murine cells) |
| TGFβ | Immunosuppression, fibrosis | Moderate |
| CCL20 | Recruitment of pro-tumorigenic leukocytes | High |
Combine RNA sequencing and ELISA to quantify chemokine expression post-stimulation .
Validate functional impact using siRNA knockdown or neutralizing antibodies.
Murine models showed reduced tumor burden with IL-36Ra, but human pharmacokinetic (PK) predictions require adjusting for interspecies differences in receptor expression (e.g., IL-36R levels in female mice vs. male humans) .
Use semi-mechanistic PK/PD models incorporating:
Backbone recombination: Merge fragments from natural antibodies to stabilize nonideal features (e.g., CDR loops) .
Sequence optimization: Balance stability and binding energy using Rosetta design calculations .
| Design Cycle | Expression Improvement | Key Adjustment |
|---|---|---|
| 1 | Low | Baseline algorithm |
| 5 | High | Added sequence/structure constraints |
Design antibodies targeting conserved epitopes (e.g., IL-36R) with enhanced affinity and reduced immunogenicity .