Tumor necrosis factor-α promoter polymorphism TNF2 is associated with a stronger delayed-type hypersensivity reaction in the skin of borderline tuberculoid leprosy patients

Moraes, Milton Ozório; Duppré, Nádia Cristina; Suffys, Philip Noël; Santos, Adalberto Rezende; Almeida, Alexandre S. de; Nery, José A. C.; Sampaio, Elizabeth P.; Sarno, Euzenir Nunes

doi:10.1007/s002510000295

Cited by 43 publications

(29 citation statements)

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“…85-87 A significant association of TNF À308A was found in borderline tuberculoid leprosy patients with the magnitude of in vivo delayed type hypersensitivity skin test reactivity to cutaneously injected M. leprae antigens. 88 TNF SNPs may be associated with inflammatory leprosy nerve damage, but this has not been investigated in large numbers of patients thus far. 89 More recent studies have shown that signalling deficient mutations in certain Toll like receptors (notably TLR2), which act upstream of TNF can be strongly associated with lepromatous leprosy, implicating among others, a role for TNF.…”

Section: Leprosymentioning

confidence: 99%

Is there a future for TNF promoter polymorphisms?

2004

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The in vitro study of TNF promoter polymorphism (SNP) function was stimulated by the numerous case-control (association) studies of the polymorphisms in relation to human disease and the appearance of several studies claiming to show a functional role for these SNPs provided a further impetus to researchers interested in the role of TNF in their disease of interest. In this review we consider case-control studies, concentrating on the autoimmune and inflammatory diseases rheumatoid arthritis, multiple sclerosis, ankylosing spondylitis, and asthma, and on infectious diseases including malaria, hepatitis B and C infection, leprosy and sepsis/septic shock. We also review the available evidence on the functional role of the various TNF promoter polymorphisms. In general, case-control studies have produced mixed results, with little consensus in most cases on whether any TNF polymorphisms are actually associated with disease, although results have been more consistent in the case of infectious diseases, particularly malaria. Functional studies have also produced mixed results but recent work suggests that the much studied À308G/A polymorphism is not functional, while the function of other TNF polymorphisms remains controversial. Studies of the TNF region are increasingly using extended haplotypes that can better capture the variation of the MHC region.

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Section: Leprosymentioning

confidence: 99%

Is there a future for TNF promoter polymorphisms?

2004

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“…Evidence of a provoked reversion of the specific anergy to M. leprae observed in LL cells has been reported, having motivated attempts at therapeutic interventions in the past [12,13]. M. leprae components, genetic background and long-lasting antigen stimulation are among the factors capable of explaining the anergy observed in LL patients [14,15]. Secretions from the adherent cells of LL patients have been shown to inhibit lymphocyte proliferation in healthy volunteers [16].…”

Section: Introductionmentioning

confidence: 99%

The role of indoleamine 2, 3-dioxygenase in lepromatous leprosy immunosuppression

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Lara

Amadeu

et al. 2011

Clinical and Experimental Immunology

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“…32 Furthermore, Brazilian leprosy patients that carry the TNF*2 allele have greater skin inflammatory responses to lepromin than those that do not; 75 thus, in Brazil it appears that increased production of TNFa may be important for inducing protective immune responses against leprosy.…”

Section: Class III Regionmentioning

confidence: 99%

Genetics of susceptibility to leprosy

2002

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The ancient disease of leprosy can cause severe disability and disfigurement and is still a major health concern in many parts of the world. Only a subset of those individuals exposed to the pathogen will go on to develop clinical disease and there is a broad clinical spectrum amongst leprosy sufferers. The outcome of infection is in part due to host genes that influence control of the initial infection and the host's immune response to that infection. Identification of the host genes that influence host susceptibility/resistance will enable a greater understanding of disease pathogenesis. In turn, this should facilitate development of more effective therapeutics and vaccines. So far at least a dozen genes have been implicated in leprosy susceptibility and a genome-wide linkage study has lead to the identification of at least one positional candidate. These findings are reviewed here.

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Tumor necrosis factor-α promoter polymorphism TNF2 is associated with a stronger delayed-type hypersensivity reaction in the skin of borderline tuberculoid leprosy patients

Cited by 43 publications

References 0 publications

Is there a future for TNF promoter polymorphisms?

Is there a future for TNF promoter polymorphisms?

The role of indoleamine 2, 3-dioxygenase in lepromatous leprosy immunosuppression

Genetics of susceptibility to leprosy

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