The function of the CD2 protein is abnormal in multiple sclerosis.

Area of Science:

• Immunology
• Neuroimmunology
• Cellular Immunology

Background:

• T cell adhesion to sheep red blood cells (SRBC) is mediated by the CD2 protein.
• This adhesion and subsequent T cell activation are crucial immune functions.
• Deficiencies in these processes are observed in active multiple sclerosis (MS).

Purpose of the Study:

• To investigate T cell adhesion and activation through the CD2 protein in leukocytes from MS patients.
• To compare CD2-mediated immune responses in MS patients versus healthy controls.
• To explore the role of prostaglandins in T cell adhesion defects in MS.

Main Methods:

• Flow cytometry (FACS) was used to measure CD2 antigen expression on T cells.
• Mononuclear cells (MNC) from MS patients and controls were assessed for avid T cell (TA) formation (binding >= 10 SRBC).
• T cell activation and proliferation were induced using specific monoclonal antibodies (mAb 9-1 and mAb 9.6) targeting CD2.

Main Results:

• MS patients formed significantly fewer avid T cells (TA) compared to controls.
• CD2 antigen expression was equivalent between MS and control groups, both at baseline and after activation.
• While controls showed decreased TA% after in vitro prostaglandin exposure, MS cells did not, suggesting refractoriness.
• Indomethacin treatment increased TA% in MS cells, supporting the role of endogenous prostaglandins.
• T cell proliferation upon CD2 stimulation was significantly diminished in MS patients.

Conclusions:

• Despite normal CD2 expression on T cells, MS patients exhibit defective T cell adhesion to SRBC and impaired activation through the CD2 pathway.
• Prostaglandins may contribute to reduced T cell adhesion in MS, potentially due to endogenous production.
• These findings highlight a functional deficit in CD2-mediated T cell responses in multiple sclerosis.