Carbohydrate Differences in HLA-DR Molecules Synthesized by Alveolar Macrophages and Blood Monocytes^1–3

Abstract

Two-dimensional gel electrophoresis was used to compare immunoprecipitated, radiolabeled HLA-DR molecules synthesized by alveolar macrophages (AM) and blood monocytes (BM) of the same healthy, nonsmoking volunteers. No charge differences were noted by isoelectric focusing. Molecular weight analysis of HLA-DR from AM revealed a complex pattern of radioactive spots differing slightly in molecular weight. This pattern was apparent in both the alpha and the beta chains. In contrast, a simpler pattern without the slight molecular weight differences was noted in HLA-DR from BM. The differences were eliminated by labeling AM and BM in the presence of tunicamycin, a specific inhibitor of protein-carbohydrate linkages of the N-glycosidic type. Thus, it appears that neutral, N-linked carbohydrate moieties account for the differences in HLA-DR molecules between AM and BM. The differential glycosylation of HLA-DR molecules in AM and BM may relate to mononuclear phagocyte development as well as antigen-presenting function.

Accessory Cell Function of Human Alveolar Macrophages in Antigen-Induced T Lymphocyte Proliferation

“…The molecular weights of these antigens were identical to those reported previously [5,11,26]. Two-dimensional gel electrophoresis of these anti gens showed similar results to the report by Ferro et al [27],…”

Macrophages in Innate and Acquired Immunity

“…[53][54][55] Furthermore, AMs inhibit the potent AC capabilities of dendritic cells. 56 Potential explanations include differences in HLA-DR (human leukocyte antigen-DR) expression, 57 differences in arachidonic acid metabolism, 58 secretion of inhibitory cytokines, 38 co-secretion of inhibitors of T cell proliferation [e.g., nitric oxide (NO)], [59][60][61] expression of inhibitory surface molecules, 62 and failure to express co-stimulatory molecules (e.g., B7). 63 Figure 3 Sites of pulmonary immune responses.…”

Defective antigen presentation by lavage cells from terminal patients with cystic fibrosis

“…The suppressor subset reduces the antigen-presenting capacity of the other [8], although it has also been suggested that the poor antigen-presenting function is due to defective expression of the B7 costimulatory molecules [9]. Most AM express cell surface MHC class II molecules, although there are reported to be differences in the glycosylation pattern of MHC class II antigens between AM and circulating monocytes [10] and between normal AM and those from patients with interstitial lung disease [11]. AM can stimulate allogeneic T cells, though autologous T cells only weakly, in a mixed leucocyte reaction (MLR) [12].…”