1,638 research outputs found
Coccidiosis in chickens and other birds
Cover title."Revision of Bulletin 411.
Further investigations of the transmission of fowl paralysis (Neurolymphomotosis) by direct transfusion
Publication authorized August 24 1945.Digitized 2007 AES.Includes bibliographical references (page 18)
Coccidiosis in chickens and other birds
Cover title."Bulletin 512 revised.
Trichomoniasis of turkeys
Cover title."A revision of Bulletin 456"--P. [3]
Coccidiosis in chickens and other birds
Cover title."Bulletin 372 revised"--Cover
Studies on the origin and transmission of fowl paralysis (Neurolymphomatosis) by blood inoculation
Publication authorized August 19, 1939.Digitized 2007 AES.Includes bibliographical references (pages 18-23)
Regulatory T Cells Prevent Th2 Immune Responses and Pulmonary Eosinophilia during Respiratory Syncytial Virus Infection in Mice
During viral infection, inflammation and recovery are tightly controlled by competing proinflammatory and regulatory immune pathways. Respiratory syncytial virus (RSV) is the leading global cause of infantile bronchiolitis, which is associated with recurrent wheeze and asthma diagnosis in later life. Th2-driven disease has been well described under some conditions for RSV-infected mice. In the present studies, we used the Foxp3(DTR) mice (which allow specific conditional depletion of Foxp3(+) T cells) to investigate the functional effects of regulatory T cells (Tregs) during A2-strain RSV infection. Infected Treg-depleted mice lost significantly more weight than wild-type mice, indicating enhanced disease. This enhancement was characterized by increased cellularity in the bronchoalveolar lavage (BAL) fluid and notable lung eosinophilia not seen in control mice. This was accompanied by abundant CD4(+) and CD8(+) T cells exhibiting an activated phenotype and induction of interleukin 13 (IL-13)- and GATA3-expressing Th2-type CD4(+) T cells that remained present in the airways even 14 days after infection. Therefore, Treg cells perform vital anti-inflammatory functions during RSV infection, suppressing pathogenic T cell responses and inhibiting lung eosinophilia. These findings provide additional evidence that dysregulation of normal immune responses to viral infection may contribute to severe RSV disease
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