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1.
Mucosal Immunol ; 7(2): 239-48, 2014 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-23778354

RESUMO

Immunity to Nippostrongylus brasiliensis reinfection requires pulmonary CD4⁺ T-cell responses. We examined whether secondary lymphoid recruited or pre-existing lung CD4⁺ T-cell populations coordinated this immunity. To do this, we blocked T-cell egress from lymph nodes using Fingolimod (FTY720). This impaired host ability to resolve a primary infection but did not change effectiveness of recall immunity. Associated with this effective recall immunity was the expansion and T helper type 2 polarization of a pre-existing pulmonary CD4⁺ T-cell population. LTßR-Ig (lymphotoxin beta-receptor fusion protein)-mediated disruption of stromal cell organization of immune cells did not disrupt this recall immunity, suggesting that protection was mediated by a pulmonary interstitial residing CD4⁺ T-cell population. Adoptive transfer of N. brasiliensis-experienced pulmonary CD4⁺ T cells from FTY720-treated wild-type or T-cell interleukin (IL)-4Rα-deficient mice demonstrated protection to be IL-4Rα dependent. These results show that pre-existing CD4⁺ T cells can drive effective recall immunity to N. brasiliensis infection independently of T-cell recruitment from secondary lymphoid organs.


Assuntos
Linfócitos T CD4-Positivos/imunologia , Memória Imunológica , Subunidade alfa de Receptor de Interleucina-4/metabolismo , Pulmão/imunologia , Pulmão/metabolismo , Nippostrongylus/imunologia , Infecções por Strongylida/imunologia , Infecções por Strongylida/metabolismo , Animais , Linfócitos T CD4-Positivos/metabolismo , Movimento Celular/genética , Movimento Celular/imunologia , Modelos Animais de Doenças , Expressão Gênica , Subunidade alfa de Receptor de Interleucina-4/genética , Pulmão/parasitologia , Linfonodos/imunologia , Linfonodos/metabolismo , Camundongos , Camundongos Knockout , Infecções por Strongylida/genética , Infecções por Strongylida/parasitologia
2.
Mucosal Immunol ; 4(1): 83-92, 2011 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-20737001

RESUMO

Nippostrongylus brasiliensis infections generate pulmonary pathologies that can be associated with strong T(H)2 polarization of the host's immune response. We present data demonstrating N. brasiliensis-driven airway mucus production to be dependent on smooth muscle cell interleukin 4 receptor-α (IL-4Rα) responsiveness. At days 7 and 10 post infection (PI), significant airway mucus production was found in IL-4Rα(-/lox) control mice, whereas global knockout (IL-4Rα(-/-)) and smooth muscle-specific IL-4Rα-deficient mice (SM-MHC(Cre) IL-4Rα(-/lox)) showed reduced airway mucus responses. Furthermore, interleukin (IL)-13 and IL-5 cytokine production in SM-MHC(Cre) IL-4Rα(-/lox) mice was impaired along with a transient reduction in T-cell numbers in the lung. In vitro treatment of smooth muscle cells with secreted N. brasiliensis excretory-secretory antigen (NES) induced IL-6 production. Decreased protein kinase C (PKC)-dependent smooth muscle cell proliferation associated with cell cycle arrest was found in cells stimulated with NES. Together, these data demonstrate that both IL-4Rα and NES-driven responses by smooth muscle cells make important contributions in initiating T(H)2 responses against N. brasiliensis infections.


Assuntos
Subunidade alfa de Receptor de Interleucina-4/imunologia , Pneumopatias Parasitárias/imunologia , Miócitos de Músculo Liso/imunologia , Miócitos de Músculo Liso/metabolismo , Nippostrongylus/imunologia , Infecções por Strongylida/imunologia , Células Th2/imunologia , Animais , Ciclo Celular/genética , Citometria de Fluxo , Interleucina-13/biossíntese , Interleucina-13/imunologia , Subunidade alfa de Receptor de Interleucina-4/genética , Subunidade alfa de Receptor de Interleucina-4/metabolismo , Interleucina-5/biossíntese , Interleucina-5/imunologia , Interleucina-6/biossíntese , Interleucina-6/imunologia , Pneumopatias Parasitárias/patologia , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Knockout , Muco/metabolismo , Nippostrongylus/patogenicidade , Proteína Quinase C/metabolismo , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Transdução de Sinais , Infecções por Strongylida/patologia
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