TNF2, a polymorphism of the tumour necrosis-α gene promoter, is a component of the celiac disease major histocompatibility complex haplotype

1996 ◽  
Vol 26 (9) ◽  
pp. 2113-2118 ◽  
Author(s):  
Ross Mc Manus ◽  
Anthony G. Wilson ◽  
John Mansfield ◽  
Donald G. Weir ◽  
Gordon W. Duff ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Celiac Disease ◽  
Tumour Necrosis ◽  
Gene Promoter ◽  
Major Histocompatibility ◽  
Major Histocompatibility Complex Haplotype ◽  
Histocompatibility Complex

scholarly journals Major Histocompatibility Complex Haplotype Determines hsp70-Dependent Protection against Measles Virus Neurovirulence

2009 ◽  
Vol 83 (11) ◽  
pp. 5544-5555 ◽  
Author(s):  
Thomas Carsillo ◽  
Mary Carsillo ◽  
Zachary Traylor ◽  
Päivi Rajala-Schultz ◽  
Phillip Popovich ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Measles Virus ◽  
Protective Role ◽  
Major Histocompatibility ◽  
Major Histocompatibility Complex Haplotype ◽  
Brain Infection ◽  
Histocompatibility Complex ◽  
The Impact

ABSTRACT In vitro studies show that hsp70 promotes gene expression for multiple viral families, although there are few reports on the in vivo significance of virus-hsp70 interaction. Previously we showed that hsp70-dependent stimulation of Edmonston measles virus (Ed MeV) transcription caused an increased cytopathic effect and mortality in transgenic hsp70-overexpressing C57BL/6 mice (H-2 b ). The response to MeV infection is influenced by the major histocompatibility complex haplotype; H-2 d mice are resistant to brain infection due to robust antiviral immune responses, whereas H-2 b mice are susceptible due to deficiencies in this response. We therefore tested the hypothesis that the outcome of MeV-hsp70 interaction may be dependent upon the host H-2 haplotype. The impact of selective neuronal hsp70 overexpression on Ed MeV brain infection was tested with congenic C57BL/10 H-2 d neonatal mice. In this context, hsp70 overexpression conferred complete protection against virus-induced mortality, compared to >30% mortality in nontransgenic mice. Selective depletion of T-cell populations showed that transgenic mice exhibit a diminished reliance on T cells for protection. Brain transcript analysis indicated enhanced innate immune activation and signaling through Toll-like receptors 2 and 4 at early times postinfection for transgenic infected mice relative to those for nontransgenic infected mice. Collectively, results suggest that hsp70 can enhance innate antiviral immunity through Toll-like receptor signaling, supporting a protective role for physiological responses that enhance tissue levels of hsp70 (e.g., fever), and that the H-2 haplotype determines the effectiveness of this response.

scholarly journals Non-Major Histocompatibility Complex Control of Antibody Isotype and Th1 versus Th2 Cytokines during Experimental Infection of Mice with Mycobacterium avium

2001 ◽  
Vol 69 (3) ◽  
pp. 1708-1713 ◽  
Author(s):  
Vijaya Nagabhushanam ◽  
Christina Cheers
Keyword(s):  
Major Histocompatibility Complex ◽  
Antibody Response ◽  
Mycobacterium Avium ◽  
Enzyme Linked Immunosorbent Assay ◽  
Similar Response ◽  
Th2 Cytokines ◽  
Major Histocompatibility ◽  
Major Histocompatibility Complex Haplotype ◽  
Histocompatibility Complex ◽  
Ifn Γ

ABSTRACT Infection of different strains of mice withMycobacterium avium has revealed genetic control of the immunoglobulin isotype induced and of the balance between Th1 and Th2 cytokines. Female BALB/c or C57BL/10 mice were infected intranasally with 105 M. avium organisms. The antibody response was measured over 18 weeks by enzyme-linked immunosorbent assay and Western blotting, while numbers of cytokine-producing cells were assessed at 12 to 15 weeks by ELISPOT assay. Upon infection, C57BL/10 mice produced a clear Th1 response with strong gamma interferon (IFN-γ) production, no interleukin-4 (IL-4), and almost entirely immunoglobulin G2a (IgG2a) antibody. In contrast, BALB/c mice developed T cells producing IL-4, as well as those producing IFN-γ, while the antibody response was a mixture of IgG1 and IgG2a. Antibodies from BALB/c mice were also able to recognize a greater range of antigens than were C56BL/10 mice. B10D2 mice, which carry the BALB/c major histocompatibility complex haplotype on a C57BL/10 background, followed the C57BL/10 cytokine pattern. Mice infected withListeria monocytogenes did not show a similar response dichotomy.

Tumour necrosis factor and lymphotoxin genes map close to H–2D in the mouse major histocompatibility complex

Nature ◽  
1987 ◽  
Vol 325 (6101) ◽  
pp. 265-267 ◽  
Author(s):  
Urs Müller ◽  
C. Victor Jongeneel ◽  
Sergei A. Nedospasov ◽  
Kirsten Fischer Lindahl ◽  
Michael Steinmetz
Keyword(s):  
Major Histocompatibility Complex ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Major Histocompatibility ◽  
Mouse Major Histocompatibility Complex ◽  
Histocompatibility Complex ◽  
Necrosis Factor
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