Adhesion molecule expression patterns indicate activation and recruitment of CD4+ T cells from the lymph node to the peripheral blood of early cutaneous leishmaniasis patients

Abstract

Adhesion molecules play a crucial role in cell migration and recruitment. Expression of adhesion molecules that preferentially address cells to inflammatory sites is a critical event in the formation and maintenance of leishmaniasis lesions. In this work, we analyzed the expression of CD11a, CD11b and CD62L, adhesion molecules involved in cell activation and circulation, in CD4+ and CD8+ T cells from peripheral blood and lymph nodes of patients with early cutaneous leishmaniasis. The percentage of expression of CD62L, CD11a and CD11b in total lymphocytes was lower in lymph nodes as compared to peripheral blood. Moreover, differences in adhesion molecule expression between blood and lymph nodes were more striking in CD4+ than CD8+ T cells. Stimulation of PBMC from leishmaniasis patients with soluble Leishmania antigens (SLA) lead to the expansion of CD4+CD62Lhigh cells, CD4+CD11b+ cells and to an increase in the intensity of expression of CD11a in CD4+, but not CD8+ T cells. Our data suggest that early activation events that occur in the lymph nodes of patients recently infected with Leishmania lead to changes in T cell adhesion molecule expression, favoring migration to the periphery and increasing the likelihood of further recruitment to lesion sites.

Clinical and immunopathological spectrum of American cutaneous leishmaniasis with special reference to the disease in Amazonian Brazil: a review

“…In consequence, T cells recruited from the peripheral blood to the inflamatory infiltrate of mucosal lesions (the focus of leishmanial infection) are preferentially primed to operate as Th1 cytokines (IFN-γ, IL-2 and TNF-α, principally). In this respect, Costa et al (2003) have recently demonstrated the role of adhesion molecules (CD11a, CD11b and CD62L) in determining the preferential address of T cells to inflamatory sites of leishmaniasis lesions, especially their effect on the highest expression of CD11a in CD4+ T cells. This raises speculations regarding the possible role of adhesion molecules in promoting a CD4+ Th1 immune activation by L. (V.) braziliensis.…”

The skin homing receptor cutaneous leucocyte-associated antigen (CLA) is up-regulated byLeishmaniaantigens in T lymphocytes during active cutaneous leishmaniasis

“…In situ analyses have shown high levels of LFA1a-and LFA-1b-positive cells in the dermis of leishmaniasis patients, although expressed differentially in CL and diffuse cutaneous leishmaniasis [28]. High percentages of activated cells expressing CD62L high , LFA-1a and LFA-1b are found in peripheral blood in comparison to the lymph nodes of CL patients in the early stages of the disease, suggesting that these cells are available for recruitment to lesion sites [15]. The percentage of skin cells presenting CLA is very low, comprising less than one-third of the cells from CL [14,29], which is surprising considering the high percentage of memory T cells in the inflammatory infiltrate [4].…”

“…The percentage of skin cells presenting CLA is very low, comprising less than one-third of the cells from CL [14,29], which is surprising considering the high percentage of memory T cells in the inflammatory infiltrate [4]. Differences in the expression of migration molecules in CD4 + and CD8 + T cells indicate that there are specific requirements for the homing of these cells to a leishmaniasis lesion [13,15,26]. However, it is not known whether CD4 + or CD8 + T cells express CLA differentially in leishmaniasis lesions and blood.…”

Proteins of Leishmania (Viannia) shawi confer protection associated with Th1 immune response and memory generation

“…In order to evaluate the frequencies of memory T cells in immunized mice, T lymphocytes were phenotyped with the markers CD62L and CD45RB. CD62L is an adhesion molecule associated with the activation and circulation of activated lymphocytes [46,47]. CD45RB is an important molecule associated with TCR activation [48] and its expression is reduced following T lymphocyte activation.…”