Open AccessMucosal macrophage subsets of the gut in HIV: decrease in antigen‐presenting cell phenotype
Author(s) -
LIM S. G.,
CONDEZ A.,
POULTER L. W.
Publication year - 1993
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1993.tb03418.x
Subject(s) - immunology , phenotype , macrophage , antigen , biology , human immunodeficiency virus (hiv) , mucosal immunology , medicine , immune system , immunity , in vitro , genetics , gene
SUMMARY The effect of HIV infection on intestinal lamina propria macrophage subsets was investigated in 41 patients at various stages of HIV infection (asymptomatic HIV infection, n = 17; AIDS, n = 24). Duodenal biopsies taken from HIV patients at endoscopy were snap frozen and cryostat sections cut for immunohistochemical staining. MoAbs CD68 (EBM11. pan‐macrophage marker). RFD1 (antigen‐presenting cells) and RFD7 (mature phagocytic macrophages) were used to identify cell subsets using indirect immunoperoxidase or alkaline phosphatase. Double immunofluoresccncc using MoAbs to HIV proteins (p24, p17 and gp120) and RFD1 were used to identify HIV‐infected antigen‐presenting cells. Double immunofluoresccncc was also used to identify macrophages that expressed both RFD1 and RFD7 (‘suppressor’ macrophages). Intensity of HLA‐DR expression in lamina propria cells was investigated using a MoAb to HLA‐DR directly conjugated to glucose oxidase. The results show that there was no difference in overall density of macrophages, but there was a significant decrease in dendritic cells (RFD1 + ) in all clinical stages of HIV. There was no difference in the density of RFD7 + macrophages, nor was there a difference in intensity of HLA‐DR expression in lamina propria cells. Only four HIV‐infected cells were positively identified in the 41 patients. This result suggests that the antigen‐presenting arm of mucosal immune defences may be seriously compromised in HIV infection, and represents a further insult to mucosal immunity already impaired as a result of loss of CD4 + T lymphocytes. This may contribute to development of opportunist infection in the gut.