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


     
 

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
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
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nishikomori, R.
Right arrow Articles by Strober, W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nishikomori, R.
Right arrow Articles by Strober, W.
The Journal of Immunology, 2001, 166: 6776-6783.
Copyright © 2001 by The American Association of Immunologists

BALB/c Mice Bearing a Transgenic IL-12 Receptor {beta}2 Gene Exhibit a Nonhealing Phenotype to Leishmania major Infection Despite Intact IL-12 Signaling

Ryuta Nishikomori*, Sanjay Gurunathan{dagger}, Kanako Nishikomori* and Warren Strober1,*

* Mucosal Immunity Section and {dagger} Clinical Immunology Section, Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892

In BALB/c mice infected with Leishmania major, early secretion of IL-4 leads to a Th2-type response and nonhealing. We explored the role of IL-4-induced down-regulation of the IL-12R{beta}2 chain in the establishment of this Th2 response. First, we showed that the draining lymph nodes of resistant C57BL/6 mice infected with L. major were enriched in CD4+/IL-12R{beta}2 chain+ cells producing IFN-{gamma}. Next, we demonstrated that BALB/c background mice bearing an IL-12R{beta}2-chain transgene manifested a nonhealing phenotype similar to wild-type littermates despite the persistence of their ability to undergo STAT4 activation. Finally, we found that such transgenic mice display more severe infection than wild-type littermates when treated with IL-12 7 days after infection, and under this condition, the mice display increased Leishmania Ag-induced IL-4 secretion. These studies indicate that although CD4+/IL-12R{beta}2 chain+ T cells are important components of the Th1 response, maintenance of IL-12R{beta}2 chain expression is not sufficient to change a Th2 response to a Th1 response in vivo and thus to allow BALB/c mice to heal L. major infection.




This article has been cited by other articles:


Home page
 J. Immunol.Home page
A. P. Nigg, S. Zahn, D. Ruckerl, C. Holscher, T. Yoshimoto, J. M. Ehrchen, F. Wolbing, M. C. Udey, and E. von Stebut
Dendritic Cell-Derived IL-12p40 Homodimer Contributes to Susceptibility in Cutaneous Leishmaniasis in BALB/c Mice
J. Immunol., June 1, 2007; 178(11): 7251 - 7258.
[Abstract] [Full Text] [PDF]

Home page
 Antimicrob. Agents Chemother.Home page
Y. Charoenvit, G. T. Brice, D. Bacon, V. Majam, J. Williams, E. Abot, H. Ganeshan, M. Sedegah, D. L. Doolan, D. J. Carucci, et al.
A Small Peptide (CEL-1000) Derived from the {beta}-Chain of the Human Major Histocompatibility Complex Class II Molecule Induces Complete Protection against Malaria in an Antigen-Independent Manner
Antimicrob. Agents Chemother., July 1, 2004; 48(7): 2455 - 2463.
[Abstract] [Full Text] [PDF]

Home page
 JEMHome page
E. von Stebut, J. M. Ehrchen, Y. Belkaid, S. L. Kostka, K. Molle, J. Knop, C. Sunderkotter, and M. C. Udey
Interleukin 1{alpha} Promotes Th1 Differentiation and Inhibits Disease Progression in Leishmania major-susceptible BALB/c Mice
J. Exp. Med., July 21, 2003; 198(2): 191 - 199.
[Abstract] [Full Text] [PDF]

Home page
 Infect. Immun.Home page
P. Kropf, S. Herath, R. Klemenz, and I. Muller
Signaling through the T1/ST2 Molecule Is Not Necessary for Th2 Differentiation but Is Important for the Regulation of Type 1 Responses in Nonhealing Leishmaniamajor Infection
Infect. Immun., April 1, 2003; 71(4): 1961 - 1971.
[Abstract] [Full Text]

Home page
 J. Immunol.Home page
G.-X. Zhang, B. Gran, S. Yu, J. Li, I. Siglienti, X. Chen, M. Kamoun, and A. Rostami
Induction of Experimental Autoimmune Encephalomyelitis in IL-12 Receptor-{beta}2-Deficient Mice: IL-12 Responsiveness Is Not Required in the Pathogenesis of Inflammatory Demyelination in the Central Nervous System
J. Immunol., February 15, 2003; 170(4): 2153 - 2160.
[Abstract] [Full Text] [PDF]

Home page
 Infect. Immun.Home page
J. Li, U. M. Padigel, P. Scott, and J. P. Farrell
Combined Treatment with Interleukin-12 and Indomethacin Promotes Increased Resistance in BALB/c Mice with Established Leishmania major Infections
Infect. Immun., October 1, 2002; 70(10): 5715 - 5720.
[Abstract] [Full Text] [PDF]

Home page
 Infect. Immun.Home page
F. Aguilar Torrentera, J. D. Laman, M. Van Meurs, L. Adorini, E. Muraille, and Y. Carlier
Endogenous Interleukin-12 Is Critical for Controlling the Late but Not the Early Stage of Leishmania mexicana Infection in C57BL/6 Mice
Infect. Immun., September 1, 2002; 70(9): 5075 - 5080.
[Abstract] [Full Text] [PDF]

Home page
 JEMHome page
L. Gorelik, S. Constant, and R. A. Flavell
Mechanism of Transforming Growth Factor {beta}-induced Inhibition of T Helper Type 1 Differentiation
J. Exp. Med., June 3, 2002; 195(11): 1499 - 1505.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 2001 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 2001 by The American Association of Immunologists, Inc. All rights reserved.