Expression and distribution of CD11a/CD18 and CD54 during human T cell-B cell interactions.
Interactions between intercellular adhesion molecule 1 (ICAM-1, CD54) and leukocyte function-associated antigen 1 (LFA-1, CD11a/CD18) play a critical role in T cell-B cell collaboration. The current experiments were carried out to determine the expression and distribution of these adhesion molecules on human peripheral T cells and B cells during T cell-B cell collaboration. Resting CD4+ T cells were largely ICAM-1 negative, whereas immobilized anti-CD3 monoclonal antibody (mAb) rapidly induced ICAM-1 expression. By contrast, most B cells expressed ICAM-1 before activation, and further increases in density were noted with stimulation. Both B cells and CD4+ T cells expressed LFA-1 before activation, although the density on CD4+ T cells was considerably greater. A double staining method for electron microscopic analysis was developed that permitted analysis of the expression and distribution of ICAM-1 to be assessed during T cell-B cell collaboration. Under the experimental conditions examined, B cells showed a uniform distribution of ICAM-1. In contrast, ICAM-1 was highly mobile on the surface of CD4+ T cells. If the T cells were not fixed, staining, even at 4 degrees C, caused rapid redistribution of ICAM-1 into aggregates. However, by fixing cells before the staining procedures, the distribution of ICAM-1 on CD4+ T cells could be accurately assessed. Most (85%) of the fixed activated CD4+ T cells showed a uniform distribution of ICAM-1. However, when activated CD4+ T cells were cocultured with B cells, redistribution of ICAM-1 on CD4+ T cells but not B cells occurred, such that the majority (85%) was found at or immediately adjacent to the point of attachment to the B cells. No redistribution of LFA-1 on either T cells or B cells was found. These findings suggest that rapid changes in density of ICAM-1 expression and the mobility of ICAM-1 on activated T cells may play a role in providing activation signals to B cells during T cell-B cell collaboration.
Harold C. Simmons Arthritis Research Center, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75235.
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S
Tohma
J E
JE
Ramberg
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PE
Lipsky
D015703:Antigens, CD / Q000032:analysis* / Q000276:immunology; D001402:B-Lymphocytes / Q000166:cytology* / Q000276:immunology; D018821:CD18 Antigens; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D015815:Cell Adhesion Molecules / Q000032:analysis* / Q000276:immunology / Q000502:physiology; D002450:Cell Communication / Q000276:immunology*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1; D008213:Lymphocyte Activation; D016169:Lymphocyte Function-Associated Antigen-1 / Q000032:analysis* / Q000276:immunology* / Q000502:physiology; D008854:Microscopy, Electron; D013601:T-Lymphocytes / Q000166:cytology* / Q000276:immunology
D015703:Antigens, CD; D018821:CD18 Antigens; D015815:Cell Adhesion Molecules; D016169:Lymphocyte Function-Associated Antigen-1; D018799:Intercellular Adhesion Molecule-1