Participação de células B-1 na rejeição de aloenxertos no camundongo
Arquivos
Data
2009
Tipo
Tese de doutorado
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Resumo
Na ausência de estímulo antigênico, células B-1 são importantes produtoras de
anticorpos naturais em camundongos e humanos e são consideradas como a
primeira linha de defesa contra patógenos. Por causa disso, o papel dessas
células em respostas imunes mediadas por células T é comumente
negligenciado. No entanto recentemente foram descritas participações de
células B-1 nas hipersensibilidades tardia e imediata. O presente trabalho
verificou o papel de células B-1 na rejeição aguda de aloenxertos no
camundongo, um processo orquestrado por células T. Para tal, foram
transplantados coração e pele alogênicos para camundongos selvagens e
camundongos deficientes em células B-1. A cinética de rejeição, as células
infiltrantes no enxerto e a migração de células B-1 foram analisadas. Foi
observado um atraso na cinética de rejeição do camundongo deficiente em
células B-1, quando comparado com o camundongo selvagem. A transferência
adotiva de células B-1 eliminou tal atraso. A sobrevida estendida do enxerto foi
concomitante com menos células T CD8+
e mais mastócitos infiltrantes no
enxerto. Células B-1 foram encontradas infiltrando o enxerto poucos dias após
os transplantes. Os resultados deste trabalho mostram que há uma
participação de células B-1 na rejeição aguda de aloenxertos e colaboram para
o entendimento da biologia dessas células.
B-1 B cells are important producers of natural antibodies in mice and humans and, therefore, are considered as the first line of defense against pathogens. Because of that, their role in T-cell mediated immune responses is commonly underrated. However, recent studies have described the participation of B-1 cells in immediate and delayed-type hypersensitivity. The present work assessed the role of B-1 cells in the rejection of allografts in mice, an immune reaction mainly orchestrated by T cells. We have transplanted allogeneic skin and heart to wild-type and B-1 cell-deficient mice, and followed rejection kinetics. Skin graft-infiltrating cells were analyzed by flow cytometry. We observed a delay in rejection kinetics of B-1 cell-deficient mice when compared to wild-type mice. Adoptive transfer of B-1 cells into B-1 cell-deficient mice abrogated this delay. The longer survival observed in the absence of B-1 cells correlated with less CD8+ T cells infiltrating the grafts, as well as with more mast cells. Collectively, our results show the participation of B-1 cells in the allograft rejection process in mice, thus collaborating to the understanding of B- 1 cell biology.
B-1 B cells are important producers of natural antibodies in mice and humans and, therefore, are considered as the first line of defense against pathogens. Because of that, their role in T-cell mediated immune responses is commonly underrated. However, recent studies have described the participation of B-1 cells in immediate and delayed-type hypersensitivity. The present work assessed the role of B-1 cells in the rejection of allografts in mice, an immune reaction mainly orchestrated by T cells. We have transplanted allogeneic skin and heart to wild-type and B-1 cell-deficient mice, and followed rejection kinetics. Skin graft-infiltrating cells were analyzed by flow cytometry. We observed a delay in rejection kinetics of B-1 cell-deficient mice when compared to wild-type mice. Adoptive transfer of B-1 cells into B-1 cell-deficient mice abrogated this delay. The longer survival observed in the absence of B-1 cells correlated with less CD8+ T cells infiltrating the grafts, as well as with more mast cells. Collectively, our results show the participation of B-1 cells in the allograft rejection process in mice, thus collaborating to the understanding of B- 1 cell biology.
Descrição
Citação
MARTINS, Mauro Fantini Nogueira. Participação de células B-1 na rejeição de aloenxertos no camundongo. 2009. 112 f. Tese (Doutorado em Ciências) - Escola Paulista de Medicina, Universidade Federal de São Paulo (UNIFESP), São Paulo, 2009.