Tissue distribution of rat macroglobulins in tumour‐bearing rats

Journal of Leukocyte Biology

Rowland

et al. 2005

Section: Discussionmentioning

confidence: 99%

Expression of the common heat-shock protein receptor CD91 is increased on monocytes of exposed yet HIV-1-seronegative subjects

Kebba

Journal of Leukocyte Biology

Rowland

et al. 2005

“…Thus, levels of a CD91 ligand, ␣ 2 -macroglobulin, are elevated in animal models of cancer 47 and during the recovery of animals from autoimmune encephalitis. 48 Indeed, the infusion of animals with ␣ 2 -macroglobulin protects them from experimental autoimmune disease.…”

Section: Resultsmentioning

confidence: 99%

The heat-shock protein receptor CD91 is up-regulated in monocytes of HIV-1–infected “true” long-term nonprogressors

Gazzard

Kim

et al. 2003

Blood

A small proportion of patients with human immunodeficiency virus type 1 (HIV-1) remains asymptomatic for a long period after infection. It is thought that a vigorous immune response may contribute to long-term nonprogression, though studies are confounded by heterogeneity among patients. We studied the levels of HIV-1 receptors, costimulatory T-cell molecules, and dendritic cell (DC) numbers in 18 patients with long-term infection, CD4 counts greater than 400 cells/mm 3 , and HIV-1 viral loads lower than 50 copies/mL. These patients were further differentiated through the presence or absence of 2-LTR DNA circles, a possible marker for residual ongoing HIV-1 replication. A statistically significant increase in levels of CD91, the heat-shock protein (HSP) receptor, was observed in therapy-naive patients who had no evidence of ongoing viral replication (P ‫؍‬ .01). This difference was most notable on their monocytes. High levels of CD91 may be a host factor that contributes to the maintenance of long-term nonprogression. The ability of CD91 to internalize ␣-defensins and to cross-present exogenous antigen to cytotoxic T lymphocytes through major histocompatibility complex (MHC) class 1 may maintain CD8 ؉ responses in these patients. (Blood. 2003;101:4000-4004)

“…Pathways regulating expression of CD91 are poorly understood, although correlative evidence exists for downregulation of CD91-mediated immune activation as a mechanism of immune escape. Thus levels of a CD91 ligand, a 2-macroglobulin, are elevated in animal models of cancer [16], and during recovery of animals from autoimmune encephalitis [17]. Indeed, infusion of animals with a 2-macroglobulin prevents experimental autoimmune pathology.…”

Section: Discussionmentioning

confidence: 99%

The common heat shock protein receptor CD91 is up-regulated on monocytes of advanced melanoma slow progressors

Clinical and Experimental Immunology

Bower

Gazzard

et al. 2004

SUMMARYDespite advances in our understanding of tumour immunology there is no therapy of proven survival benefit for advanced melanoma. Nevertheless, disease progression is slow in a small proportion of patients with metastatic melanoma, suggesting a contribution to outcome from host factors. Recent data have indicated the importance of the heat shock protein receptor CD91 in immune responses to, and progression of, infectious disease. Here we investigate the relationship between CD91 expression and outcome in malignancy. Rare melanoma patients were recruited with advanced disease that was progressing unusually slowly. CD91 expression on their monocytes was compared with control patients with more typical rapidly advancing metastatic disease. Th1 and Th2 cytokines, as well as innate and adaptive immune subsets, were also measured in the two groups. A significant increase in median CD91 expression levels was observed in slow progressors ( P = 0·006). There were no differences in other immune subset markers or inflammatory cytokines. The ability of CD91 to internalize and cross-present tumour antigens through the major histocompatibility complex class I pathway may maintain CD8-positive cytotoxic T cell responses and contribute to slow progression of advanced melanoma.