Genetic aspects and microenvironment affect expression of CD18 and VLA-4 in experimental tuberculosis.
Control of infection by Mycobacterium tuberculosis is dependent on macrophage activation and efficient migration of effector T-cell populations. Lymphocyte differentiation is associated with changes in cell surface phenotype and alterations in the migratory pattern of these cells. In this study, we investigated the expression of adhesion receptors involved in activation and migration process in experimental tuberculosis. We observed that susceptible BALB/c mice infected with virulent M. tuberculosis by intraperitoneal route presented downmodulation of very late antigen 4 (VLA-4) and unchanged levels of CD18 and CD44hi on peritoneal lymphocytes. On the other hand, lymphocytes from resistant C57BL/6 mice infected by the same route showed unchanged levels of VLA-4 and upregulation of CD18 and CD44hi. However, when BALB/c mice were infected by intratracheal route, lung lymphocytes presented a different pattern of CD18, CD44hi and VLA-4 expression from that observed on peritoneal cells, characterized by unchanged levels of VLA-4 and upregulation of CD18 and CD44hi- coincidentally the same phenotype found on peritoneal cells from C57BL/6. These results suggest that susceptibility and resistance to M. tuberculosis infection, depending on the experimental model, are related to the expression of CD18, CD44hi and VLA-4. Moreover, the microenvironment at the site of infection seems to differentially regulate the expression of these receptors. Thus, the up- or downmodulation of these adhesion receptors is probably associated with differential recruitment of T cells at the site of infection, which may or may not mediate protection in experimental tuberculosis.
Bonato
V L D
VL
REDE-TB, Department of Biochemistry and Immunology, School of Medicine of Ribeirão Preto, University of São Paulo, São Paulo, Brazil.
Goncalves
E D C
ED
Santos
R R
RR
Silva
C L
CL
D000818:Animals; D001202:Ascitic Fluid / Q000276:immunology / Q000473:pathology; D018821:CD18 Antigens / Q000378:metabolism*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000473:pathology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology / Q000473:pathology; D002454:Cell Differentiation; D002465:Cell Movement; D018960:Hyaluronan Receptors / Q000378:metabolism; D039041:Integrin alpha4beta1; D016023:Integrins / Q000378:metabolism*; D008168:Lung / Q000276:immunology / Q000473:pathology; D008213:Lymphocyte Activation; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D014395:Peritonitis, Tuberculous / Q000235:genetics* / Q000276:immunology* / Q000473:pathology; D016201:Receptors, Lymphocyte Homing / Q000378:metabolism*; D013045:Species Specificity; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000473:pathology; D014397:Tuberculosis, Pulmonary / Q000235:genetics* / Q000276:immunology* / Q000473:pathology
D018821:CD18 Antigens; D018960:Hyaluronan Receptors; D039041:Integrin alpha4beta1; D016023:Integrins; D016201:Receptors, Lymphocyte Homing