The JI
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     
 


This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gonzalo, J. A.
Right arrow Articles by Martinez-A, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gonzalo, J. A.
Right arrow Articles by Martinez-A, C.

The Journal of Immunology, Vol 157, Issue 8 3298-3304, Copyright © 1996 by American Association of Immunologists


ARTICLES

Enterotoxin septic shock protection and deficient T helper 2 cytokine production in growth hormone transgenic mice

JA Gonzalo, R Mazuchelli, M Mellado, JM Frade, AC Carrera, C von Kobbe, I Merida and C Martinez-A
Department of Immunology and Oncology, National Center of Biotechnology, CSIC, University Autonoma, Madrid, Spain.

Neuroendocrine hormones have long been thought to play a role in lymphoid development and function. In particular, growth hormone has been shown to mediate thymic development as well as to promote T cell engraftment in severe combined immunodeficiency mice. Murine T helper cells are classified into two subsets based on their cytokine production pattern. Here, we report that transgenic mice for bovine growth hormone show significant alterations in T cell function and decreased capability for cytokine production, an effect that is more acute in T helper cells as measured by their inability to produce IL-4 upon in vivo injection with Staphylococcus aureus enterotoxin B. Furthermore, upon immunization with conventional Ags, growth hormone transgenic mice produce an altered Ig isotype pattern characterized by a response shift from IgG1 in nontransgenic mice to IgG2 in transgenic mice. The impaired T cell responses correlated with survival from septic shock mediated by bacterial enterotoxins. We conclude that growth hormone may have the potential of regulating immune responses in pathologic processes associated with hyperactivation of T cells or with massive cytokine production.


This article has been cited by other articles:


Home page
J. Biol. Chem.Home page
R. Garzon, S. F. Soriano, J. M. Rodriguez-Frade, L. Gomez, A. Martin de Ana, M. Sanchez-Gomez, C. Martinez-A, and M. Mellado
CXCR4-mediated Suppressor of Cytokine Signaling Up-regulation Inactivates Growth Hormone Function
J. Biol. Chem., October 22, 2004; 279(43): 44460 - 44466.
[Abstract] [Full Text] [PDF]


Home page
J. Exp. Med.Home page
S. F. Soriano, P. Hernanz-Falcon, J. M. Rodriguez-Frade, A. M. de Ana, R. Garzon, C. Carvalho-Pinto, A. J. Vila-Coro, A. Zaballos, D. Balomenos, C. Martinez-A., et al.
Functional Inactivation of CXC Chemokine Receptor 4-mediated Responses through SOCS3 Up-regulation
J. Exp. Med., August 5, 2002; 196(3): 311 - 321.
[Abstract] [Full Text] [PDF]


Home page
Mol. Endocrinol.Home page
G. Luo and L.-y. Yu-Lee
Stat5b Inhibits NF{kappa}B-Mediated Signaling
Mol. Endocrinol., January 1, 2000; 14(1): 114 - 123.
[Abstract] [Full Text]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1996 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1996 by The American Association of Immunologists, Inc. All rights reserved.