RESUMO
IL-7 is a crucial factor for the development of lymphocytes, and it is absolutely necessary for γδ T cells. Mice deficient in L-7 have a deficit of B and αß T lymphocytes, and an absence of mature γδ TCR cells. IL-7 is essential for the survival, development and maturation of Schistosoma sp., although its production is associated with protection against intestinal helminths. The presence of anti-Anisakis simplex antibodies, especially IgA, is related to a lower frequency in CD3 + CD56 + αß + lymphocytes and all subpopulations of γδ T cells. In this work, the relationship of IL-7 with humoral and cellular responses against A. simplex in 100 healthy subjects was studied. We have found significantly higher IL-7 levels in anti-A. simplex IgA-positive subjects (p < 0.001). The positivity of anti-A. simplex IgA was associated with a significant reduction in the frequency of CD3 + αß+ (p < 0.01), CD3 + CD4 + αß+, CD3 + CD8 + αß+, CD3 + CD56 + αß+, CD3 + γδ+, CD3 + CD4-CD8-γδ+ and CD3 + CD56 + γδ+ (p < 0.05) cells. In the case of NKT cells, this same phenomenon was also associated with IgE positivity. There was a weak inverse correlation (Spearman) of IL-7 levels with the frequencies of CD3 + CD4 + αß+ (-0.125, p = 0.047), CD3 + CD8 + αß+ (-0.204, p = 0.032), CD3 + CD56 + αß+ (-0.247, p = 0.007), CD3 + γδ+ (-0.267, p = 0.007), CD3 + CD4-CD8-γδ+ (-0.266, p = 0.003), and CD3 + CD8 + γδ + (-0.302, p = 0.002) cells. The role of NKT cells in the anti-A. simplex response was confirmed and an association between IL and 7 levels and specific antibodies, especially IgA, was demonstrated. The higher production of IL-7 would represent a compensatory mechanism in response to the reduction in lymphocyte populations associated with the response against this parasite.
Assuntos
Anisakis , Receptores de Antígenos de Linfócitos T gama-delta , Animais , Humanos , Imunoglobulina A , Interleucina-7 , Camundongos , Receptores de Antígenos de Linfócitos T alfa-beta , Subpopulações de Linfócitos TRESUMO
AIMS: The objective of this investigation is to evaluate the mechanisms Anisakis simplex employs to modify its host immune system, regarding the larval antigens interactions with Toll-Like-Receptors (TLRs). METHODS AND RESULTS: In a previous study, we described that the stimulation of bone marrow derived dendritic cells (BMDCs) with A. simplex larval antigens drive an acute inflammatory response in BALB/c mice, but a more discrete and longer response in C57BL/6J. Moreover, when A. simplex larval antigens were combined with TLR agonists (TLR 1/2-9), they modified mainly TLR2, TLR4 and TLR9 agonists responses in both mice strains, and also TLR3, TLR5 and TLR7 in BALB/c. Antigen-presenting ability was analyzed by the detection of CD11c + cells expressing surface markers (CD80-86, MHC I-II), intracellular cytokines (IL-10, IL-12, TNF-α) and intracellular proteins (Myd88, NF-κß) by Flow Cytometry. Secreted IL-10 was measured by ELISA. CONCLUSION: Our findings confirm not only that the host genetic basis plays a role in the development of a Th2/Th1/Treg response, but also it states A. simplex larval antigens present specific mechanisms to modify the innate response of the host. As allergies share common pathways with the immune response against this particular helminth, our results provide a better understanding into the specific mechanisms of A. simplex allergy related diseases.