The complement receptor 3, CR3 (CD11b/CD18), on T lymphocytes: activation-dependent up-regulation and regulatory function

Abstract

The complement receptor 3 (CR3; CD11b/CD18) is present exclusively on leukocytes, particularly on NK cells, monocytes and polymorphonuclear neutrophils. Approximately 10% of peripheral T lymphocytes and, as we found now mainly CD8+ cells, expressed CD11b. Upon stimulation, however, expression of CD11b was up‐regulated also on CD4+ cells. Stimulation of T cells either bycross‐linked anti‐CD3 and IL‐2 or by mononuclear cells and mitogen yielded up to 28% CD11b+ T cells. The majority of CD11b+ T cells also expressed CD56. T cell lines established from healthy donors were also found to express CR3. When restimulated up to 90% of cells became positive for CD11b making those cells an ideal tool for studying the functional role of CD11b. Antibodies to CD11b and bona fide ligands for the complement receptor inhibited the anti‐CD3‐induced T cell proliferation and as well as IL‐2 release . In contrast, proliferation of a CD11b– T cell line was not inhibited. Taken together, our data indicate an activation‐dependent expression of the complement receptor on T cells and suggest a regulatory function.

Differences in T‐cell responses between Mycobacterium tuberculosis and Mycobacterium africanum‐infected patients

“…These were mostly cytotoxic CD8 + T cells expressing CD56 as previously described [17], with significantly lower production of cytokines (IL-2, IFN-γ, and TNF-α) in Mafcompared with Mtb-infected patients posttreatment. This result is in agreement with a previous study, which describes that activation induced increased CD11b expression by CD3 + T cells result in inhibition of proliferation and reduced IL-2 secretion [17].…”

“…These were mostly cytotoxic CD8 + T cells expressing CD56 as previously described [17], with significantly lower production of cytokines (IL-2, IFN-γ, and TNF-α) in Mafcompared with Mtb-infected patients posttreatment. This result is in agreement with a previous study, which describes that activation induced increased CD11b expression by CD3 + T cells result in inhibition of proliferation and reduced IL-2 secretion [17]. Therefore, CD11b + being a marker of T-cell activation and trafficking [14,16], might indicate an unrecovered immune profile in Maf-infected patients, or incomplete clearance of bacilli despite treatment completion and negative AFB in sputum.…”

“…Recent studies have shown CD11b expression by highly activated T cells that are mainly cytotoxic [16,17]. Following gating on the lymphocyte population, activated T cells were defined as CD3 + CD11b + cells and the proportions of IFN-γ, IL-2, and TNF-α positive subsets within this population were determined.…”

“…Following flow cytometry analysis, three patients had poor quality data at baseline; therefore, data from 18 Maf-and 27 Mtb-infected patients were examined before treatment. Thirty-three patients were successfully followed up after treatment (14)(15)(16)(17)(18)(19); all were sputum acid-fast bacilli (AFB) smearnegative after 6 months of treatment. …”

Surface profiles of live colorectal cancer cells and tumor infiltrating lymphocytes from surgical samples correspond to prognostic categories

“…Hierarchical cluster analysis of the 11 CRC and TIL antigens produced similar groups of patients that were separated into three categories (relapse-free, systemic relapse, and cancer-specific death), supporting the hypothesis that surface antigen profiles on CRC cells and TIL yield prognostic information. (Wagner et al, 2001;Shelley et al, 2002;Lee et al, 2010).…”