CD18 is the β subunit of the β2 integrin family, forming heterodimers with CD11a, CD11b, CD11c, or CD11d to create leukocyte adhesion molecules (e.g., LFA-1, Mac-1). These integrins mediate:
Cell adhesion to endothelial cells via ICAM-1 (CD54) or ICAM-2 (CD102).
Immune cell migration and activation during inflammation.
Signal transduction in T cells and neutrophils.
CD18 deficiency causes leukocyte adhesion deficiency type 1 (LAD1), characterized by recurrent infections and impaired wound healing.
Clone M18/2
Target: Mouse CD18.
Applications:
Flow cytometry (0.5 µg/test).
Blocking leukocyte adhesion in functional assays.
Detected in splenocytes and bone marrow cells.
Clone TS1/18
Target: Human CD18.
Applications:
Flow cytometry, immunohistochemistry, and immunocytochemistry.
Endotoxin levels ≤10 EU/mg.
Clone 68-5A5
Target: Human CD18.
Function: Blocks LFA-1/ICAM-1 interactions.
Reactivity: Human leukocytes.
Preclinical Studies
Study Model
Intervention
Outcome
Source
Canine myocardial infarction
Anti-CD18 (R15.7)
↓ Infarct size by 44% (p=0.008); ↑ LV ejection fraction (43.6% vs. 28.5%)
In vitro T cell activation
Anti-CD18 antibody
Blocked off-target T cell activation by 50–70% (p<0.01)
Clinical Trials
LIMIT AMI Trial (2001)
Mechanistic Insights
Off-Target T Cell Activation: High-affinity CD3 bispecific antibodies (BsAbs) induce cytokine release syndrome (CRS). CD18 blockade reduces CRS risk by inhibiting LFA-1/ICAM-1 interactions without compromising antitumor activity.
Structural Role: Only 20–33% of CDR residues directly bind antigens; non-contact residues optimize paratope conformation.
Challenges and Limitations
Clinical Efficacy: Anti-CD18 therapies show promise in animal models but limited success in human trials (e.g., LIMIT AMI).
Infection Risk: Trends toward increased bacterial infections were noted with rhuMAb CD18 (p=0.33).