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Articles by M. J Holtzman
Total Records ( 2 ) for M. J Holtzman
  R Tachdjian , C Mathias , S Al Khatib , P. J Bryce , H. S Kim , F Blaeser , B. D O'Connor , D Rzymkiewicz , A Chen , M. J Holtzman , G. K Hershey , H Garn , H Harb , H Renz , H. C Oettgen and T. A. Chatila

Polymorphisms in the interleukin-4 receptor chain (IL-4R) have been linked to asthma incidence and severity, but a causal relationship has remained uncertain. In particular, a glutamine to arginine substitution at position 576 (Q576R) of IL-4R has been associated with severe asthma, especially in African Americans. We show that mice carrying the Q576R polymorphism exhibited intense allergen-induced airway inflammation and remodeling. The Q576R polymorphism did not affect proximal signal transducer and activator of transcription (STAT) 6 activation, but synergized with STAT6 in a gene target– and tissue-specific manner to mediate heightened expression of a subset of IL-4– and IL-13–responsive genes involved in allergic inflammation. Our findings indicate that the Q576R polymorphism directly promotes asthma in carrier populations by selectively augmenting IL-4R–dependent signaling.

  B. T Edelson , W KC , R Juang , M Kohyama , L. A Benoit , P. A Klekotka , C Moon , J. C Albring , W Ise , D. G Michael , D Bhattacharya , T. S Stappenbeck , M. J Holtzman , S. S. J Sung , T. L Murphy , K Hildner and K. M. Murphy

Although CD103-expressing dendritic cells (DCs) are widely present in nonlymphoid tissues, the transcription factors controlling their development and their relationship to other DC subsets remain unclear. Mice lacking the transcription factor Batf3 have a defect in the development of CD8+ conventional DCs (cDCs) within lymphoid tissues. We demonstrate that Batf3–/– mice also lack CD103+CD11b DCs in the lung, intestine, mesenteric lymph nodes (MLNs), dermis, and skin-draining lymph nodes. Notably, Batf3–/– mice displayed reduced priming of CD8 T cells after pulmonary Sendai virus infection, with increased pulmonary inflammation. In the MLNs and intestine, Batf3 deficiency resulted in the specific lack of CD103+CD11b DCs, with the population of CD103+CD11b+ DCs remaining intact. Batf3–/– mice showed no evidence of spontaneous gastrointestinal inflammation and had a normal contact hypersensitivity (CHS) response, despite previous suggestions that CD103+ DCs were required for immune homeostasis in the gut and CHS. The relationship between CD8+ cDCs and nonlymphoid CD103+ DCs implied by their shared dependence on Batf3 was further supported by similar patterns of gene expression and their shared developmental dependence on the transcription factor Irf8. These data provide evidence for a developmental relationship between lymphoid organ–resident CD8+ cDCs and nonlymphoid CD103+ DCs.

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