Genetics and pulmonary medicine bullet  3: Genetic susceptibility to tuberculosis in human populations

Bellamy, Richard

doi:10.1136/thx.53.7.588

Cited by 77 publications

(48 citation statements)

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“…That microevolutionary principles can help explain the incidence, pathology and characteristics of many human diseases has not gone unnoticed by the medical community [10–12]. This is particularly evident in studies in which population genetics have been applied to uncover the causes of disease susceptibility in human populations [13–18]. One intriguing and insightful application of microevolutionary principles to the study of cancer was recently put forward by Greaves and Malley [7].…”

Section: The Prospective Power Of Microevolutionmentioning

confidence: 99%

Cellular Hyperproliferation and Cancer as Evolutionary Variables

Alvarado

2012

Current Biology

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Technological advances in biology have begun to dramatically change the way we think about evolution, development, health and disease. The ability to sequence the genomes of many individuals within a population, and across multiple species, has opened the door to the possibility of answering some long-standing and perplexing questions about our own genetic heritage. One such question revolves around the nature of cellular hyperproliferation. This cellular behavior is used to effect wound healing in most animals, as well as, in some animals, the regeneration of lost body parts. Yet at the same time, cellular hyperproliferation is the fundamental pathological condition responsible for cancers in humans. Here, I will discuss why microevolution, macroevolution and developmental biology all have to be taken into consideration when interpreting studies of both normal and malignant hyperproliferation. I will also illustrate how a synthesis of evolutionary sciences and developmental biology through the study of diverse model organisms can inform our understanding of both health and disease.

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Section: The Prospective Power Of Microevolutionmentioning

confidence: 99%

Cellular Hyperproliferation and Cancer as Evolutionary Variables

Alvarado

2012

Current Biology

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“…Human leukocyte antigen alleles Some authors have reported an association between human leukocyte antigens (HLAs) and susceptibility to TB, principally the class I antigens A10 and B8 and the class II antigen DR2 (DRB1*1501) [97]. HLA genotyping of HIV-positive patients with disseminated MAC has revealed positive associations with the DR2, DQB1*0601 and DRB1*0701 alleles, and a negative association with the DMA*0102 allele [98].…”

Section: Other Primary Immunodeficiency Disordersmentioning

confidence: 99%

Susceptibility to nontuberculous mycobacterial lung disease: Table 1—

Sexton¹,

Harrison²

2008

Eur Respir J

143

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The nontuberculous mycobacteria (NTM) exhibit heterogeneous pathogenicity in humans. Articles on known and potential human factors capable of producing susceptibility to NTM lung disease (NTMLD) were identified by a systematic search of the medical literature, and are reviewed in the present study.Patients with pre-existing structural lung disease are known to be at risk of NTMLD. Other susceptible groups have become recognised since the 1980s, in particular middle-aged nonsmokers without previous lung disease (a group including those with Lady Windermere syndrome) and patients with genetically determined defects of cell-mediated immunity, including abnormalities of the interleukin-12/interferon-c axis, certain human leukocyte antigen alleles, cystic fibrosis transmembrane conductance regulator mutations, and polymorphisms of solute carrier 11A1 (or natural resistance-associated macrophage protein 1) and the vitamin D receptor.Information is also accruing about acquired systemic causes of susceptibility to NTMLD, including inhibitory antibodies directed against interferon-c, post-menopausal waning of endogenous oestrogen levels, coeliac disease and exposure to use of dietary phyto-oestrogens. It is not known whether immunosuppressive factors, such as oral corticosteroid treatment, chronic renal failure, diabetes mellitus and other known risk factors for pulmonary tuberculosis, are also risk factors for the development of NTMLD. Caution is appropriate in managing such patients.

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“…Interestingly, some clinical forms of tuberculosis have been related with specific alleles of class II and class I molecules. An association with HLA-DR2 and particularly with its subtype DR15 in linkage disequilibrium with DQ5 has been found in patients with smearpositive pulmonary tuberculosis (Bellamy, 1998). This observation has been refined using DNA based HLA typing and it was confirmed a link with genes DRB1*1501 and DQB1*0502 (Meyer et al, 1998).…”

Section: Role Of Genetic Factors In the Immunopathology Of Takayasu'smentioning

confidence: 71%