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Table of Contents   
ORIGINAL ARTICLE  
Year : 2012  |  Volume : 5  |  Issue : 4  |  Page : 307-312
Racial differences in susceptibility to infection by Mycobacterium tuberculosis


Department of Internal Medicine, S. Johannes Hospital, Germany

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Date of Web Publication8-Oct-2012
 

   Abstract 

Background: The prevalence of tuberculosis among blacks is known to be higher than among whites. The basis for these differences remains unclear. The purpose of this paper is to review the literature and evaluate the data which bears on the question of racial differences in susceptibility to tuberculosis. Materials and Methods: Systematic review of peer reviewed studies identified through Medline. The search was restricted to articles published in English. The references of the identified papers for further relevant publications were also reviewed. Results: For the review, 31 papers were eligible from 417 identified in the search. The prevalence of TB among black skin people was 81.5% and 18.5% in white skin people. The black subjects demonstrated higher frequency of the Fok1 E2-C4T F allele, Bsm1 E8-G-+ 284A- B allele, APa1 e9-T-48G- a allele, and Taq1 E9-T-32C- t allele and marked differences in IL-6, IL-10, TNF-α, TGF-β, and IFN-γ than white subject. There were no significant differences in MCP-1 2518 A, G allele between black and white subjects. White subjects tended to have borderline significantly higher mean serum of vitamin D (58.4 nmol/l) than black subjects (37.7 nmol/l). The capacities of skin to synthesize vitamin D Post-UVB were significantly higher in whites than in black subjects. Conclusions: Black skin people had consistently higher susceptibility to infection by M. tuberculosis than are whites skin peoples. The mechanism of a racial difference in infectibility by M. tuberculosis is the result of a complex interaction between the environmental, immunologic, and genetic factors.

Keywords: African, caucasian, ethnicity, race, tuberculosis

How to cite this article:
Fares A. Racial differences in susceptibility to infection by Mycobacterium tuberculosis. Ann Trop Med Public Health 2012;5:307-12

How to cite this URL:
Fares A. Racial differences in susceptibility to infection by Mycobacterium tuberculosis. Ann Trop Med Public Health [serial online] 2012 [cited 2018 May 22];5:307-12. Available from: http://www.atmph.org/text.asp?2012/5/4/307/102032

   Introduction Top


Despite reductions in the global burden of tuberculosis (TB), the great majority of TB incidence remains higher among certain racial/ethnic minorities. The basis for the different rates of TB among various ethnocultural populations remains unclear. TB is a multifactorial disorder in which the environment interacts with host-related factors, contributing to the overall clinical spectrum. [1] Improved understanding of the individual balance between degree of exposure and inherited genetic susceptibility to infection, as well as the respective effects of environmental and host-related factors on the development of disease, will have strong implications for TB control and prevention. [2] The present study designs combining different research methods, but it offers the advantage of assessing together the roles of environmental, immunologic, and genetic factors in susceptibility to infection by Mycobacterium tuberculosis and disease development.


   Materials and Methods Top


Search strategy

Electronic databases, MEDLINE, EMBASE, and Cochran Library, were used in this review to identified peer-reviewed relevant studies up to June 1, 2011 with keywords TB, Race, Ethnicity, African, Caucasian OR Vitamin, Race, Ethnicity, African, and Caucasian. The electronic search was tailored to each database in order to locate articles that met the eligibility criteria as described below. Relevant publications and epidemiological data were also downloaded from websites of international agencies such as World Health Organisation (WHO) or online peer-review journal such as American Journal of Clinical Nutrition and Journal of Metabolism and Endocrinology. In addition, the bibliographies of the relevant articles identified through the searches for any additional articles that met the inclusion criteria were reviewed. No contact was made with authors of the papers.

Eligibility criteria

Sources were screened for relevance to the topic, originality, a well-described methodology, rigor of statistical analysis, and an adequate sample size, where relevant. Sources were excluded where sample size was inadequate (except in qualitative studies), methodology was not well described, statistical analysis was unclear, and where the full article was unavailable. In addition, only papers published in English language were considered and dealt with human subjects. Studies dealing with brown skin color like Hispanic, Asian, or Chinese subjects were excluded. Studies deals with health subjects were included; subject with conditions known to be associated with vitamin D deficiency (e.g., rickets and osteoporosis) were excluded. In some cases, control groups of healthy subjects exist in studies of home nursing residents or subjects with condition known to be associated with vitamin D deficiency; in these cases, control groups were included in the study. Some of the studies reported random selection of population-based participants in all age, gender, and ethnic groups, and another studies reported random selection participants in selected age and gender strata, in these cases black and white skin groups were included in the study. In these studies we used a nmol/dl unit to express serum level of 25(OH)D; therefore, in the studies using ng/dl unit as outcome measurements of 25(OH)D was converted to nmol /dl unit.

Data abstraction

Data were abstracted from each eligible study: (1) study characteristics including the sample size and the mean follow-up time; (2) patient characteristics including mean age, age range, female and male number, and type of skin color; and (3) serum level of chemokines, cytokines, and vitamin D.


   Result Top


A total of 417 studies were identified from the initial Pubmed search. Of these articles, 31 studies met the inclusion criteria. Five of these studies investigated the prevalence of TB among black and white people. Among these, 81.5% of black skin people were TB positive, while 18.5% of white skin people were TB positive [Table 1].
Table 1: Prevelance of TB among black and white

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Four controlled BCG trials provided information on annual TB cases. The average annual TB case rates per 100,000 in these four studies were 413 among black's and 213 among white's reactors [Table 2].
Table 2: Annual TB case rates among intial Tuberclin reactor[8]

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Three studies investigated vitamin D receptor polymorphisms and susceptibility to TB among healthy subject, at a total of 101 white and 643 black subjects. The black subjects demonstrated higher frequency of the Fok1 E2-C4T F allele, Bsm1 E8-G-+ 284A- B allele, APa1 e9-T-48G- a allele, and Taq1 E9-T-32C- t allele than white subject. While white subjects had a significant higher frequency of the Fok1 E2-C4T -f allele, Bsm1 E8-G-+ 284A- b allele, APa1E9-T-48G- A allele, and Taq1 E9-T-32C- T [Table 3].
Table 3: Vitamin D receptor

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A total of 11 studies with 22,858 subjects from two racial groups (white and black) were conducted in USA and UK. White subjects tended to have borderline significantly higher mean serum of vitamin D (58.4 nmol/l) than black subjects (37.7 nmol/l) [Table 4].
Table 4: Serum Vitamin D level

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For the MCP-1 - 2518 SNP, a total of 162 white and 36 black subjects were enrolled in two studies. There were no significant differences in MCP-1 2518 A, G allele between black and white subjects [16],[30] [Table 5].
Table 5: Chemokines difference bewteen black and white subjects

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Two studies investigated the differences in serum cytokines level between black and white subjects; in one study black subjects demonstrated marked differences in the inheritance patterns for polymorphisms in several cytokine genes such as IL-6, IL-10, TNF-α, TGF-β, and IFN-γ. In another study, the proinflammatory cytokine interleukin-6 IL6-174 G/G genotype was 36.5 times more common among African Americans. IL10-1082 A/A genotype was 2.8 times more common in African-American than in the white. TNF-a did not differ significantly between African-American and white [Table 6].
Table 6: Cytokines difference bewteen black and white subjects

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Four small studies have evaluated the differing capacities of skin to absorb ultraviolet radiation (UVR) and synthesize vitamin D among black and in comparison to white subjects. One of the study conducted in USA showed the effect of increased skin pigment on the cutaneous production of vitamin D3, circulating vitamin D concentrations were determined in two Caucasian and three black volunteers after exposure to a single standard dose of UVR. Exposure of Caucasian subjects to one minimal erythemal dose (MED) of UVR greatly increased serum vitamin D concentrations by up to 60-fold 24-48 h after exposure, whereas this dose did not significantly change serum vitamin D concentrations in black subjects. Re-exposure of one black subject to a dose of UVR six times larger than the standard dose increased circulating vitamin D to concentrations similar to those recorded in Caucasian subjects after exposure to the lower dose. [33] In another study, the serum vitamin D concentrations of six dark skin Asians in response to 1.5 times their MED of whole-body UVR was studied. The mean serum vitamin D concentrations rose from a baseline of 4.98 ± 4.98 nmol/L to a peak of 94.6 ± 29.8 nmol/L at 24 h. This concentration was gradually declining back to baseline by day 9. The UVR needed to produce an MED in Asians, with their darker skin, was greater (49-133 mJ/cm 2 ) than that required in Caucasians (31-48 mJ/cm 2 ). Asians may need longer exposure to sunlight than Caucasians do to give a similar response. [34] In another study conducted among healthy young subjects from three racial groups (white, Indian, and black), following whole-body exposure to 27 mJ/cm 2 of UVB (wavelengths, 290-320 nm), there was a significant racial group effect on serum vitamin D3 levels. Post-UVB levels were significantly higher in whites (31.4 ± 4.4 nmol/L) than in Indians or blacks (12.8 ± 2.9 and 9.1 ± 2.1 nmol/L, respectively). [35] In one more study, 13 white and 7 black adults ranging from 22 to 35 years of age were submitted to sequential total body suberythemal doses of UVB (280-315 nm) biweekly for 6 weeks. Initial UVB dose was 5% below the MED for the most sensitive skin, followed by 10% increase per exposure for 4 weeks. Blood samples were drawn weekly. Baseline vitamin D concentrations were significantly lower in blacks compared to whites, but the increases in serum vitamin D concentrations were similar in both groups. [36]


   Discussion Top


The result of this review confirms the well-known fact that the prevalence of TB infection is higher among blacks than that among whites. The mechanism of a racial difference in infectibility by M. tuberculosis is the result of a complex interaction between the host and environmental factors. Several studies from different regions, ethnic groups, and cultures show positive association between the serum level of vitamin D and susceptibility to TB infection or reactivation. [37] Serum vitamin D concentrations are significantly lower in TB patients compared with those in control groups. Several mechanisms have been proposed to explain this relation, most of them concerned with the possibility of the role of active metabolite vitamin D (25-(OH) D) in the hosts defence against human TB, thus suggesting that metabolites (25-(OH) D) can act to suppress the growth of M. tuberculosis through the induction of nitric oxide (NO) production by macrophages. [38]

Despite large variation probably originating in differences in culture (clothing, time spent outdoors), vitamin D intake, genetic factors, and study-related factors such as selection of participants, and method used to determine 25(OH)D. The overall level of vitamin D in this study was significantly higher in Caucasian than African populations. Since UVB radiation from direct sunlight stimulates the production of vitamin D in humans through natural chemical reactions, people with increased levels of melanin in their skin produce much lower levels of the vitamin than those with lower levels of melanin, as those whose skin contains higher levels of melanin filtrate the sun's UVR, thereby limiting the amount of the vitamin produced through this particular mechanism. Furthermore, the most evident study about the role of melanin in immune system showed that the melanin was equally effective in inhibiting production of TNF by monocytes stimulated with the purified protein derivative of M. tuberculosis also inhibit production of IL-6 by IL-1-stimulated human fibroblasts and endothelial cells. [39] This result suggests that the people with dark or semi-dark skin are at more risk to disease development than white skin as a consequence of melanin on vitamin D production and immune system function inhibition. Therefore, vitamin D supplementation or dietary could make for a remarkably effective method for reducing the infection rate of TB in peoples of African descent. Clinical trials for TB endemic regions in Africa have been proposed to test if these laboratory results can be replicated on a larger scale and to verify if lower rates of the incidence of TB would result.

A number of polymorphisms in the human VDR gene (located on chromosome 12q12-14) have previously been associated with TB susceptibility, of which most commonly, FokI, BsmI, ApaI, and TaqI. The active metabolite of vitamin D, 1,25 dihydroxyvitamin D3, is an important immunoregulatory hormone. Its effects are exerted via the VDR, which is present on human monocytes and activated T- and B-lymphocytes. Considering the role of the VDR and it specific immunological functions, including activation of monocytes, stimulation of cell-mediated immunity, and suppression of lymphocyte proliferation, immunoglobulin production and cytokine synthesis, variation in the VDR genes may contribute to disease susceptibility. However, several studies in different ethnic populations investigate the possible association of VDR gene in TB susceptibility but the result was inconsistent with specific populations. In this review, one can find similarity in the frequency of SNP Fok1 allele between Venda population (South Africa) and Gambian and that could be profound effect on susceptibility to TB in black people.

MCP-1 is suggested to play an initial role in attracting immune cells to combat TB. Several studies conducted in on different ethnic groups strongly suggest an influence of MCP-1 variation on TB susceptibility. Positive linkage of an association of MCP-1 -2581G with TB susceptibility in Mexican and Korean TB patients [40] has been observed. In contrast, no association of MCP-1 -2581 was found in Brazilian multicase families [41] and in a Chinese patient group from Hong Kong. [42] In the present study, it was found that the white subjects had no significant differences in frequency of the G and A alleles compared with black subjects. One can believe that, at present, the overall data do not sufficiently support any major involvement of that variant in TB susceptibility or protection.

TNF- α has been implicated as a key protective cytokines involved in macrophage activation and granuloma formation. [43] M. tuberculosis induces TNF-α secretion by macrophages, dentric cells, and T cells. [44] In humans, when anti-TNF-α was used to treat patients with crohn and rheumatoid arthritis, it was associated with occurrence or reactivation of M. tuberculosis leading to clinical TB. [43] The most widely studied SNP in the TNF-α gene is the G to A substitution at position-308. The high frequency of the functional SNP associated with low TNF-α production may limit effective immunity to M. tuberculosis infection in the black subjects.

IFN-γ, a classical macrophage activator, has been implicated multiple immunological function, produced by both CD4+ and CD8+ T cells, as well as by NK cells. [44] Humans defective in genes for IFN-γ or the IFN-y receptor are prone to serious mycobacterial infection. [44] The lack of IFN-γ expression was associated with deficient production of nitric oxide, nitric oxide synthase, and reactive oxygen intermediates by infected macrophage, which are thought to be key in facilitating the killing of bacilli. In the context of the present study, the high prevalence of the functional SNP associated with low IFN-γ production may develop a less efficient cytokines response, which is required to contain M tuberculosis in black subjects. [16]

The evidence data from experimental study indicate that the secretion of IL-6 by infected macrophage may contribute to the inability of immune system to eradicate M. tuberculosis by inhibiting the responses of uninfected macrophages to IFN-y. [45] Therefore, the high frequency of the functional SNP associated with high IL-6 production may limit effective immunity to M. tuberculosis in black people.

Interleukin-10 is a potent immunomodulatory cytokine that has been shown in vitro to directly or indirectly affect multiple cell types, including macrophages, monocytes, dendritic cells, CD4 T cells, and CD8 T cells. [46] The dominant function of IL-10 is to deactivate macrophages, resulting in diminished Th1 cytokine production, [46],[30] decreased production of reactive nitrogen or oxygen species, [40] and limited Ag presentation. [39] It has been also identified as a correlate of susceptibility for TB [30] in both mice and humans. [45] The high frequency of the functional SNP associated with low IL-6 production may limit effective immunity to M. tuberculosis in black people.


   Conclusion Top


Black skin people had consistently higher susceptibility to infection by M. tuberculosis than are whites skin peoples. The data also suggest that the racial differences in chemokine's and cytokines production, as well as serum vitamin D level and cutaneous vitamin D synthesis may play a vital role in protection the body from the infection by M. tuberculosis.

 
   References Top

1.Lienhardt C, Bennett S, Del Prete G, Bah-Sow O, Newport M, Gustafson P, et al. Investigation of environmental and host-related risk factors for tuberculosis in Africa. I. Methodological aspects of a combined design. Am J Epidemiol 2002;155:1066-73.  Back to cited text no. 1
    
2.Lienhardt C. From exposure to disease: The role of environmental factors in susceptibility to and development of tuberculosis. Epidemiol Rev 2001;23:288-301.  Back to cited text no. 2
[PUBMED]    
3.Stout JE, Saharia KK, Nageswaran S, Ahmed A, Hamilton CD. Racial and ethnic disparities in pediatric tuberculosis in North Carolina. Arch Pediatr Adolesc Med 2006;160:631-7.  Back to cited text no. 3
[PUBMED]    
4.Schneider E. Tuberculosis among American Indians and Alaska Natives in the United States, 1993-2002. Am J Public Health 2005;95:873-80.  Back to cited text no. 4
[PUBMED]    
5.Shemko M, Yates M, Fang Z, Gibson A, Shetty N. Molecular epidemiology of Mycobacterium tuberculosis in patients of Somalian and white ethnic origin attending an inner London clinic. Int J Tuberc Lung Dis 2004;8:186-93.  Back to cited text no. 5
[PUBMED]    
6.Centers for Disease Control and Prevention (CDC). Racial disparities in tuberculosis-selected southeastern states, 1991-2002. Racial disparities in tuberculosis-selected southeastern states, 1991-2002.  Back to cited text no. 6
    
7.Bennett DE, Courval JM, Onorato I, Agerton T, Gibson JD, Lambert L, et al. Prevalence of tuberculosis infection in the United States population: the national health and nutrition examination survey, 1999-2000. Am J Respir Crit Care Med 2008;177:348-55.   Back to cited text no. 7
[PUBMED]    
8.Kushigemachi M, Schneiderman LJ, Barrett E. Racial differences in susceptibility to tuberculosis: Risk of disease after infection. J Chronic Dis 1984;37:853-62.  Back to cited text no. 8
    
9.Comstock GW, Woolpert SF, Livesay VT. Tuberculosis studies in Muscogee County, Georgia. Twenty - years evaluation of a community trial of BCG vaccination. Public Health Rep 1976;91:276-80.  Back to cited text no. 9
[PUBMED]    
10.Comstock GW, Shaw LW. Controlled trial of BCG vaccination in a school population: Tuberculosis studies in Muscogee County, Ga. Public Health Rep 1960;75:583-94.  Back to cited text no. 10
[PUBMED]    
11.Palmer CE, Shaw LW, Comstock GW. Community trials of BCG vaccination. Am Rev Tuberc 1958;77:877-907.  Back to cited text no. 11
[PUBMED]    
12.Comstock GW, Palmer CE. Long-term results of BCG vaccination in the southern United States. Am Rev Respir Dis 1966;93:171-83.  Back to cited text no. 12
[PUBMED]    
13.Comstock GW, Livesay VT, Woolpert SF. Evaluation of BCG vaccination among Puerto Rican children. Am J Public Health 1974;64:283-91.  Back to cited text no. 13
[PUBMED]    
14.Comstock GW, Livesay VT, Woolpert SF. The prognosis of a positive tuberculin reaction in childhood and adolescence. Am J Epidemiol 1974;99:131-8.  Back to cited text no. 14
[PUBMED]    
15.Comstock GW, Edwards LB, Livesay VT. Tuberculosis morbidity in the U.S. Navy: Its distribution and decline. Am Rev Respir Dis 1974;110:572-80.  Back to cited text no. 15
    
16.Larcombe LA, Orr PH, Lodge AM, Brown JS, Dembinski IJ, Milligan LC, et al. Functional gene polymorphisms in canadian aboriginal populations with high rates of tuberculosis. J Infect Dis 2008;198:1175-9.  Back to cited text no. 16
[PUBMED]    
17.Uitterlinden AG, Fang Y, Van Meurs JB, Pols HA, Van Leeuwen JP. Genetics and biology of vitamin D receptor polymorphisms. Gene 2004;338:143-56. Review.  Back to cited text no. 17
    
18.Bornman L, Campbell SJ, Fielding K, Bah B, Sillah J, Gustafson P, et al. Vitamin D receptor polymorphisms and susceptibility to tuberculosis in West Africa: A case-control and family study. J Infect Dis 2004;190:1631-41.  Back to cited text no. 18
[PUBMED]    
19.Matsuoka LY, Wortsman J, Chen TC, Holick MF. Compensation for the interracial variance in the cutaneous synthesis of vitamin D. J Lab Clin Med 1995;126:452-7.  Back to cited text no. 19
[PUBMED]    
20.Harris SS, Dawson-Hughes B. Seasonal changes in plasma 25-hydroxyvitamin D concentrations of young American black and white women. Am J Clin Nutr 1998;67:1232-6.  Back to cited text no. 20
[PUBMED]    
21.Looker Anne C, Dawson-Hughes B, Calvo MS, Gunter EW, Sahyoun NR. Serum 25-hydroxyvitamin D status of adolescents and adults in two seasonal subpopulations from NHANES III. Bone 2002;30:771-7.  Back to cited text no. 21
    
22.Harris SS, Soteriades E, Coolidge JA, Mudgal S, Dawson-Hughes B. Vitamin D insufficiency and hyperparathyroidism in a low income, multiracial, elderly population. J Clin Endocrinol Metab 2000;85:4125-30.  Back to cited text no. 22
[PUBMED]    
23.Harkness Laura S, Cromer Barbara A. Vitamin D deficiency in adolescent females. J Adolesc Health 2005;37:75.  Back to cited text no. 23
    
24.Dibba B, Prentice A, Laskey MA, Stirling DM, Cole TJ. An investigation of ethnic differences in bone mineral, hip axis length, calcium metabolism and bone turnover between West African and Caucasian adults living in the United Kingdom. Ann Hum Biol 1999;26:229-42.  Back to cited text no. 24
[PUBMED]    
25.McKinney K, Breitkopf CR, Berenson AB. Association of race, body fat and season with vitamin D status among young women: a cross-sectional study. Clin Endocrinol (Oxf) 2008;69:535-41.  Back to cited text no. 25
[PUBMED]    
26.Weaver CM, McCabe LD, McCabe GP, Braun M, Martin BR, Dimeglio LA, et al. Vitamin D status and calcium metabolism in adolescent black and white girls on a range of controlled calcium intakes. J Clin Endocrinol Metab 2009;94:704.  Back to cited text no. 26
    
27.Wilkins CH, Birge SJ, Sheline YI, Morris JC. Vitamin D deficiency is associated with worse cognitive performance and lower bone density in older African Americans. J Natl Med Assoc 2009;101:349-54.  Back to cited text no. 27
[PUBMED]    
28.Willis CM, Laing EM, Hall DB, Hausman DB, Lewis RD. A prospective analysis of plasma 25 -hydroxyvitamin D concentrations in white and black prepubertal females in the southeastern United States. Am J Clin Nutr 2007;85:124-30.  Back to cited text no. 28
[PUBMED]    
29.Aloia JF, Chen DG, Chen H. The 25(OH)D/PTH threshold in black women. J Clin Endocrinol Metab 2010;95:5069-73.  Back to cited text no. 29
[PUBMED]    
30.Rovin BH, Lu L, Saxena R. A novel polymorphism in the MCP-1 gene regulatory region that influences MCP-1 expression. Biochem Biophys Res Commun 1999;259:344-8.  Back to cited text no. 30
[PUBMED]    
31.Hoffmann SC, Stanley EM, Cox ED, DiMercurio BS, Koziol DE, Harlan DM, et al. Ethnicity Greatly Influences Cytokine Gene Polymorphism Distribution. Am J Transplant 2002;2:560-7.  Back to cited text no. 31
[PUBMED]    
32.Ness RB, Haggerty CL, Harger G, Ferrell R. Differential distribution of allelic variants in cytokine genes among African Americans and White Americans. Am J Epidemiol 2004;160:1033-8.  Back to cited text no. 32
[PUBMED]    
33.Clemens TL, Adams JS, Henderson SL, Holick MF. Increased skin pigment reduces the capacity of skin to synthesise vitamin D3. Lancet 1982;1:74-6.  Back to cited text no. 33
[PUBMED]    
34.Lo CW, Paris PW, Holick MF. Indian and Pakistani immigrants have the same capacity as Caucasians to produce vitamin D in response to ultraviolet irradiation. Am J Clin Nutr 1986;44:683-5.  Back to cited text no. 34
[PUBMED]    
35.Matsuoka LY, Wortsman J, Haddad JG, Kolm P, Hollis BW. Racial pigmentation and the cutaneous synthesis of vitamin D. Arch Dermatol 1991;127:536-8.  Back to cited text no. 35
[PUBMED]    
36.Brazerol WF, McPhee AJ, Mimouni F, Specker BL, Tsang RC. Serial ultraviolet B exposure and serum 25 hydroxyvitamin D response in young adult American blacks and whites: No racial differences. J Am Coll Nutr 1988;7:111-8.  Back to cited text no. 36
[PUBMED]    
37.Nnoaham KE, Clarke A. Low serum vitamin D levels and tuberculosis: A systematic review and meta-analysis. Int J Epidemiol 2008;37:113-9.  Back to cited text no. 37
[PUBMED]    
38.Rockett KA, Brookes R, Udalova I, Vidal V, Hill AV, Kwiatkowski D. 1, 25-Dihydroxyvitamin D3 induces nitric oxide synthase and suppresses growth of Mycobacterium tuberculosis in a human macrophage-like cell line. Infect Immun 1998;66:5314-21.  Back to cited text no. 38
[PUBMED]    
39.Mohagheghpour N, Waleh N, Garger SJ, Dousman L, Grill LK, Tusé D. Synthetic melanin suppresses production of proinflammatory cytokines. Cell Immunol 2000;199:25-36  Back to cited text no. 39
    
40.Flores-Villanueva PO, Ruiz-Morales JA, Song CH, Flores LM, Jo EK, Montaño M, et al. A functional promoter polymorphism in monocyte chemoattractant protein-1 is associated with increased susceptibility to pulmonary tuberculosis. J Exp Med 2005;202:1649-58.  Back to cited text no. 40
    
41.Jamieson SE, Miller EN, Black GF, Peacock CS, Cordell HJ, Howson JM, et al. Evidence for a cluster of genes on chromosome 17q11-q21 controlling susceptibility to tuberculosis and leprosy in Brazilians. Genes Immun 2004;5:46-57.  Back to cited text no. 41
[PUBMED]    
42.Chu SF, Tam CM, Wong HS, Kam KM, Lau YL, Chiang AK. Association between RANTES functional polymorphisms and tuberculosis in Hong Kong Chinese. Genes Immun 2007;8:475-9.  Back to cited text no. 42
[PUBMED]    
43.Keane J, Gershon S, Wise RP, Mirabile-Levens E, Kasznica J, Schwieterman WD, et al. Tuberculosis associated with infliximab, a tumor necrosis factor alpha-neutralizing agent. N Engl J Med 2001;345:1098-104.  Back to cited text no. 43
[PUBMED]    
44.Raja A. Immunology of Tuberculosis. Indian J Med Res 2004;120:213-32.  Back to cited text no. 44
    
45.Nagabhushanam V, Solache A, Ting L-M, Escaron CJ, Zhang JY, Ernst JD. Innate Inhibition of Adaptive Immunity: Mycobacterium tuberculosis-Induced IL-6 Inhibits Macrophage Responses to IFN-y. J Immunol. 2003; 171(9):4750-7.  Back to cited text no. 45
    
46.Thye T, Nejentsev S, Intemann CD, Browne EN, Chinbuah MA, Gyapong J, et al. MCP-1 promoter variant -362C associated with protection from pulmonary tuberculosis in Ghana. West Afr Hum Mol Genet 2009;18:381-8.  Back to cited text no. 46
[PUBMED]    

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Correspondence Address:
Auda Fares
Department of Internal Medicine, S. Johannes Hospital, Wilhelm-Busch-Straße 9, 53844 Troisdorf
Germany
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1755-6783.102032

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    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]

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