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Z Brahmi

Publications and source records attributed to Z Brahmi.

77 records · Page 5Linked to original sources

Depressed cell-mediated immunity in chronic dermatophytic infections.

The immune response was studied in ten patients with benign dermatophytosis, and in five patients with a severe affection. At the humoral level no deficiencies were observed in both groups. However, all patients showed a marked and constant increase in IgE level. Skin test response in various concentrations of antigens as well as studies of activation of lymphocytes by specific and non-specific mitogens in vitro have demonstrated a depressed cell-mediated immunity. This anergy, however, is not an "all-or-none" phenomenon; it varies and there seems to be a direct relationship between the state of anergy and the severity of the cases. Furthermore, certain discrepancies were observed between the in vivo and in vitro responses suggesting that defective cellular immune reactions in dermatophytosis may be symptomatic of a lack of some humoral factor and do not necessarily reflect an intrinsic cellular defect. Finally, among these 15 patients, 7 were brothers and sisters from 3 separate and unrelated families, suggesting an autosomal hereditary influence.

Adolescent↗

Increase in tumor necrosis factor-alpha mRNA but not perforin mRNA expression in response to two newly characterized anti-LFA-1 monoclonal antibodies.

We have generated two monoclonal antibodies (mAb), designated anti-1B11 and anti-4F9, directed to the human lymphocyte-function-associated antigen-1 (LFA-1). Indirect immunofluorescence with both mAb showed a bimodal distribution of antigen on the surface of T, natural killer (NK), and lymphokine-activated killer (LAK) cells. Neither mAb reacted with the epitopes recognized by TA1 and Mo-1 mAb on the alpha-chain of the heterodimer. Anti-1B11 and anti-4F9 immunoprecipitated polypeptide chains with molecular weights of 177 and 95 kD. Both mAb inhibited cytolytic T lymphocytes (CTL), NK, and LAK cell-mediated cytotoxicity without affecting antibody-dependent cellular cytotoxicity (ADCC). The proliferative responses of T cells to allogeneic cells were inhibited by anti-1B11 and anti-4F9, whereas the responses to phytohemagglutinin P and concanavalin A were not affected. Anti-1B11 and anti-4F9 blocked effector cell (EC)-target cell (TC) conjugate formation by 50%. Only anti-4F9 cross-reacted with LFA-1 on porcine peripheral blood lymphocytes and inhibited porcine NK, LAK, and ADCC activities. Because LFA-1 also functions at the level of signal transduction during T cell activation and we previously showed that CTL rapidly degraded perforin and tumor necrosis factor-alpha (TNF alpha) mRNA after interaction with sensitive TC, we examined the effects of the mAb on the messages for perforin and TNF alpha. Treatment of CTL with anti-1B11 and anti-4F9 induced TNF alpha message and protein levels of TNF alpha, but did not alter perforin mRNA levels.

Animals↗