Preferential Migration of Activated CD4 ⁺ and CD8 ⁺ T Cells in Response to MIP-1α and MIP-1β

Abstract

Recombinant human macrophage inflammatory protein-1 alpha (rhMIP-1 alpha) and rhMIP-1 beta were potent chemoattractants of human T lymphocytes. These rhMIP-1 cytokines attracted only T cells activated by monoclonal antibody to CD3 and did not attract unstimulated lymphocytes. Phenotypic analysis revealed that CD4+ T cells were capable of migrating in response to rhMIP-1 beta, whereas rhMIP-1 alpha induced chemotaxis of predominantly CD8+ T lymphocytes. Activated naïve and memory T cells also migrated in response to rhMIP-1 cytokines. Furthermore, these cytokines enhanced the ability of T cells to bind to an endothelial cell monolayer. These results suggest that rhMIP-1 cytokines preferentially recruit specific T cell subsets during the evolution of the immune response.

Adenovirus-mediated CD40 ligand gene-engineered dendritic cells elicit enhanced CD8+ cytotoxic T-cell activation and antitumor immunity

“…35 In addition to the chemotactic effect on T-cell migration, MIP -1 is also known to preferentially help DCs to encounter and stimulate rare tumor-specific CD8 + CTLs. 36 Therefore, up -regulation of the above cytokines and chemokines may also play a role in the enhanced antitumor immunity in this study.…”

Differential Expression of CC Chemokines and the CCR5 Receptor in the Pancreas Is Associated with Progression to Type I Diabetes

“…Collectively, these findings implicate a temporal relationship between a higher intrapancreatic MIP-1␣:MIP-1␤ ratio and the development of destructive insulitis and overt diabetes in NOD mice. Thus, although MIP-1␣ and MIP-1␤ are highly related proteins, they may have opposing functions during autoimmune inflammation (33)(34)(35).…”

“…MIP-1␣ can stimulate macrophage secretion of IL-1, IL-6, and TNF-␣, which may promote NO production by macrophages and induce Fas-mediated apoptosis of islet ␤ cells (36,37). MIP-1␣ also preferentially attracts CD8 ϩ T cells, which are required for the development of diabetes and are a source of MIP-1␣ in vivo (34,38,39). Thus, inhibition of MIP-1␣ by IL-4 may help protect islet ␤ cells from attack by effector CD8 ϩ T cells.…”

Host Responses and Antigens Involved in Protective Immunity to Mycobacterium tuberculosis

“…Pro-inflammatory cytokines (interleukin-1, IL-1; IL-6; tumour necrosis factor-a, TNF-a) and chemokines (e.g. macrophage inflammatory protein 1, interferon inducible protein 10) secreted from the infected macrophage, lead to the recruitment of monocytes and lymphocytes from the blood and the development of the inflammatory process [15][16][17][18]. This first phase of the infection is considered by Dannenberg [19] to be a symbiotic relationship between host and parasite.…”