Journal of Postgraduate Medicine
 Open access journal indexed with Index Medicus & ISI's SCI  
Users online: 14760  
Home | Subscribe | Feedback | Login 
About Latest Articles Back-Issues Articlesmenu-bullet Search Instructions Online Submission Subscribe Etcetera Contact
 :: Next article
 :: Previous article 
 :: Table of Contents
 ::  Similar in PUBMED
 ::  Search Pubmed for
 ::  Search in Google Scholar for
 ::Related articles
 ::  Article in PDF (89 KB)
 ::  Citation Manager
 ::  Access Statistics
 ::  Reader Comments
 ::  Email Alert *
 ::  Add to My List *
* Registration required (free) 

  IN THIS Article
 ::  Abstract
 ::  Materials and Me...
 ::  Results
 ::  Discussion
 ::  References
 ::  Article Tables

 Article Access Statistics
    PDF Downloaded586    
    Comments [Add]    
    Cited by others 6    

Recommend this journal


Year : 2008  |  Volume : 54  |  Issue : 1  |  Page : 7-11

Immunophenotypic characterisation of peripheral T lymphocytes in pulmonary tuberculosis

Department of Medicine, King Khalid University Hospital and College of Medicine, King Saud University, Riyadh, Saudi Arabia

Date of Submission01-Mar-2007
Date of Decision31-Oct-2007
Date of Acceptance17-Dec-2007

Correspondence Address:
A A Abba
Department of Medicine, King Khalid University Hospital and College of Medicine, King Saud University, Riyadh
Saudi Arabia
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0022-3859.39182

Rights and Permissions

 :: Abstract 

Background: The cellular immune response plays an important role in determining the outcome of infection and disease in Mycobacterium tuberculosis . Many studies of these disease interactions yield contradictory results. Aim: This study aims at determining the changes that take place in the subpopulations of T lymphocytes in the blood of patients with pulmonary tuberculosis (TB). Settings and Design: This cross-sectional study was done at King Khalid University Hospital, Riyadh, Saudi Arabia. Materials and Methods: Flow cytometry was used to determine the absolute numbers and percentages of T CD3, T CD4, T CD8, T CD19 and natural killer (NK) T cells in 54 patients with active pulmonary TB before the commencement of treatment and in 25 healthy PPD negative volunteers. Statistical Analysis: Statistical Package for Social Sciences (version 11.5) was used for analysis. Results: There were significant differences in the values of CD3, CD4 and NK T cells among the groups. The numbers of CD3 and CD4 cells were lower in subjects than in controls [1091.9 321.4 vs. 1364.6 251.2; P < 0.001 and 639.8 285 vs. 822 189.9; P < 0.004, respectively] while numbers of NK T cells were much higher in patients than in controls (410.7 286 vs. 182.3 140; P < 0.001). The numbers of CD8 cells were not significantly changed with disease (609 233.5 in subjects and 613.4 170.3 in controls P = 0.761). Conclusion: There are significant changes in the cellular immune response particularly affecting the CD3, CD4 and NK T cells with the development of pulmonary TB. Therefore, further studies of these changes may have important implications on the development of diagnostic tools, vaccines and treatment modalities.

Keywords: Immunophenotyping, pulmonary, tuberculosis, T lymphocytes

How to cite this article:
Al Majid F M, Abba A A. Immunophenotypic characterisation of peripheral T lymphocytes in pulmonary tuberculosis. J Postgrad Med 2008;54:7-11

How to cite this URL:
Al Majid F M, Abba A A. Immunophenotypic characterisation of peripheral T lymphocytes in pulmonary tuberculosis. J Postgrad Med [serial online] 2008 [cited 2023 Sep 26];54:7-11. Available from:

The burden of tuberculosis (TB) on the healthcare system remains enormous worldwide. An estimate of the annual risk of infection puts the global prevalence of TB at about 32%. [1] Of this, 5-10% go on to develop active TB. This incidence is much higher among patients co-infected with the human immune deficiency virus (HIV). [2] Active TB manifests itself within 2 years of infection in 80% of those susceptible hosts. [3] Studies have shown that the acquired immune deficiency syndrome (AIDS) is the most significant risk factor contributing to the resurgence of TB. [4] Tuberculosis remains a scourge in such areas as Africa, the Indian sub-continent and South East Asia. The ease of global travel has, amongst others, made the transmission of TB easier thereby causing resurgence in areas where reasonable degree of control was achieved. It was estimated that 1.7 million deaths occurred worldwide due to TB in 2004 alone. [5] A part of the reason for the increasing mortality is more widespread emergence of multidrug resistant tubercle bacilli. [6],[7]

Therefore, there is a need to have a proper understanding of mechanisms governing the host reaction to the pathogen. This understanding is vital to the development of vaccines and adjunctive therapies to curtail ill health and mortality due to Mycobacterium tuberculosis .

The immune response against TB is principally cell mediated. Although antibodies can be detected in infected hosts, the role of humoral immunity through B cells remains at best controversial. [8],[9] A number of cells play crucial roles in controlling the replication of M. tuberculosis once it infects a human. These include T lymphocytes, macrophages and natural killer (NK) cells. [10],[11] Activated T cells and cells from the monocytic lineage produce cytokines that regulate the immune response to the organism. Tumor necrosis α (TNF-α) in TB is produced from the pro-inflammatory monocytes that present the phenotype CD14+CD16+HLA-DR++. This cytokine is the main mediator of the pathophysiology of TB. It is essential for the limitation of bacterial dissemination, production of other immunoregulatory cytokines and maintenance of granuloma. [12] Natural killer T cells, which can be identified by the phenotype CD3+CD56+, have also been shown to participate in the immunity against TB. [13] These cells promote protection by the rapid production of IFN-γ and IL-4. [14]

Since these cells facilitate the containment of infection, it is postulated that there will be changes in the immunophenotypic characterisation of the T lymphocytes and their subpopulations in patients with active TB. Therefore, this study aims at determining whether there could be a change in the T lymphocytes and its subpopulations in patients who have active pulmonary TB.

 :: Materials and Methods Top


Fifty-four adult Saudi patients diagnosed with pulmonary TB and 25 healthy volunteers were included in the study conducted at King Khalid University Hospital Riyadh between July 2005 and June 2006. The mean age of the patients was 37.27 (SD 17.13) with a range of 13-90 years. The mean age of the control population was 36.24 (SD 6.34) with a range of 20-45 years. There are 32 (59.26%) and 15 (60%) males among the patient group and the controls, respectively. In both age and gender, there was no significant difference between the groups. The extent of disease was evaluated by the number of zones involved in a posteroanterior radiograph of the chest. A total of 18 (33.3%), 20 (37.0%), 5 (9.25%), 10 (18.5%) and 1 (1.85%) patients have involvement of 1, 2, 3, 4 and 6 zones, respectively.

All patients had symptoms of TB for at least 4 weeks and were positive for M. tuberculosis based on direct smear and/or culture of sputum. All controls had negative reaction to Mantoux test while all subjects had a positive reaction ranging from 4 to 35 mm with a mean of 17.0 5.54 mm using five tuberculin units of purified protein derivative (PPD). Both groups (controls and patients) tested negative for the HIV and had negative relevant tests for atopic and common helminthic/parasitic infections. None of the study subjects was on immunosuppressant medications. Approval for the study was obtained from the Ethical Committee of the Centre for Medical Research of King Saud University and informed consent was obtained from individual subjects and controls.

Immunophenotypic analysis

Blood samples were collected in EDTA tubes and analyzed within 6 h of storage at room temperature. The monoclonal antibodies used for this study which include mouse anti-human CD3 flourescein isothiocyanate (FITC), CD19 phycoerythrin (PE), CD4 FITC, CD4 PE, NK Cells PE and HLA-DR PE were obtained from Becton Dickinson Immunocytometry Systems (San Jose, CA, USA). Appropriate immunoglobulin G1 and Ig Ga flourochrome-conjugated antibodies used as isotype controls were also obtained from the same company. Acquisition was performed on a FACScalibur Flow Cytometer (Becton Dickinson, San Jose, CA, USA) and 3 10 4 events were collected for each sample. Analysis was performed using CELLQuest (Becton Dickinson, San Jose, CA, USA) on list mode data and the lymphocyte gate was defined forward/side scatter characteristics. For two-colour analysis, FL1/FL2 contour plots were employed to determine the level of autofluorescence and nonspecific binding.

One hundred microlitres of whole blood was mixed with 20 L of monoclonal antibodies and incubated for 15 min. Haemolysis was performed using 2 mL of commercial solution for haemolysis (FACS Lysing Solution, Becton Dickinson). After 10 min of incubation, the tubes were centrifuged to remove lysed red blood cells and washed twice with cell wash (0.015 M, pH 7.4). Peripheral blood leucocytes (PBL) were identified using monoclonal antibodies as shown in [Table - 1]. Subsets of PBL were assayed immediately by a three-colour flow cytometry. Absolute cell count was computed from the lymphocyte percentage of the differential white cell count obtained using standard laboratory procedures. The absolute count for each subset was calculated using this formula: % CD/100 x WBC (L)/100 x % lymphocytes.

Statistical analysis

Data were analyzed using Statistical Package for Social Sciences (version 11.5). Mean and SD were used to summarise continuous variables while percentages were used for categorical variables. Mann-Whitney U -test was used to investigate statistical significance between groups. The significance considered was P < 0.05.

 :: Results Top

[Table - 2] gives the results of the absolute values of CD3, CD4, CD8, CD4/CD8 ratio, CD19, NK T cells and HLA-DR among the patients with pulmonary TB and the controls. The absolute values of CD3 and CD4 are significantly lower among the patients compared to the control group ( P = 0.001 and 0.004, respectively). Although there is a difference between the mean absolute count of CD8 between the patients and the control, this portrays no statistical significance. The ratio between CD4 and CD8 cells is significantly lower among the patients compared to the control ( P = 0.007). The number of NK T cells in the peripheral blood is significantly higher in the patients than in controls ( P < 0.001). The HLA-DR is the same in the two groups. [Table - 3] details the comparison of the mean of the two groups showing similar significant differences as demonstrated by the absolute figures. The degree of lung involvement did not correlate with the changes in immunological parameters.

 :: Discussion Top

This study was undertaken to determine the changes in the mean and absolute numbers of peripheral lymphocytes in adult patients with pulmonary TB. Earlier studies have clearly demonstrated significant variations in the percentages and absolute numbers of lymphocytes and their subsets among different races, genders and age groups. [15],[16],[17] Our control population, composed of adult Saudi of mixed gender, had absolute and percent lymphocytes subpopulations comparable to earlier figures defined for the study population. [16],[18] The study shows a clear reduction in the absolute numbers and percentages of CD3 and CD4 in patients with pulmonary TB. This is reflected in the lower CD4/CD8 ratio as there is no significant difference in the CD8. The NK T cells are also significantly higher. These alterations in the cell-mediated immunity are in consonance with observations presented by other workers. [19],[20],[21] The CD4 T cells appear to exert their immunological effect through cytotoxicity against infected target cells partly by production of T cell interferon gamma (IFN-γ) and also by intern activation of the M. tuberculosis -infected macrophage which then kills the bacilli. [22],[23],[24] The reduction in CD4 has earlier been noted [25],[26] and is believed to be a result of pooling or homing of these subset of cells in the lungs. [27] Lymphocyte homing has been described in other tissues including lymph nodes [28] and pleura. [29] Our study suggests that it is principally the CD4 T cells that are homed. Tsao et al. have shown that this shift is related to the severity of pulmonary TB and is inversely related to the CD8 in the peripheral blood and bronchoalveolar lavage fluid. [30]

Another lymphocyte subset that is important in the immunity against TB is the CD8. Similar to CD4 T lymphocytes, IFN-γ production seems to be the key marker for the ability of CD8 lymphocytes to exert their cytotoxic activity in mice and humans. [31],[32] Studies in animal model have shown that deficiency of CD8 T cells can result in susceptibility to TB. [33] Our study failed to demonstrate any significant difference in the absolute count and the percentages of CD8 between the patients and control. So in this respect we differ from other studies. This difference may be related to the differences in the methods of assay. Different populations have also been shown to have differences in counts. [16],[34] Rodrigues et al. noted markedly decreased CD8 in patients with active TB which recovered after treatment. [26] They assessed the cellular activation of this population of lymphocytes by measuring the percentage of cells expressing the ectoenzyme CD38. A higher percentage of cells expressing the CD38 molecule were observed in patients with active TB which returned to control levels after therapy. So although, absolute numbers were reduced, they were at a higher level of cellular activity. Other workers have, however, noted higher numbers of CD8 which reverted to normal levels after treatment. [35],[36]

The Natural killer cells constitute a distinct subpopulation of lymphoid cells defined as CD3-, CD16+ and/or CD56+. [37] Most NK T cells in circulation are CD16+/CD56+ and are able to lyse certain target cells without the need for prior sensitisation. They are able to exert their effect before the immunity triggered by T cells comes into play and therefore of utmost importance in the initial fight against certain obligatory intracellular pathogens including M. tuberculosis . They are able to recognise the antigen independent of the α/β T cells. [38] In this study, there is a significant higher number and percentage of NK T cells in the patients compared to the controls. Our results corroborate earlier findings [34],[38],[39],[40] which indicate that input from intracellular organisms may induce expansion of NK T cells through the production of IFN-γ. The role of NK cells in mycobacterial infections is not clear, but it has been demonstrated that the activation of the innate immune response in the beginning of the infection through recruiting of pre-NK cells, could be a linkage between innate and acquired immune response. [41] The NK cells can be separated into NK bright and NK dim . The latter, which make up 90% of the NK cells, present a higher cytotoxic activity than the former. [42] Barcelos et al. [35] have shown a larger population of NK dim at the beginning of the treatment and NK bright at the end. They suggest that the cytolytic potential in these cells could be due to a higher specific activity of NK dim cells, trying to control M. tuberculosis .

Our study has not revealed any significant difference in the CD19 subpopulation underlining the small role played by the humoral system in the immunology of TB disease. Barcelos et al. [35] and Dubaniewicz et al. [43] have similar data in untreated patients. However, after treatment these cells increased significantly. It is probable that the increase is due to the endogenous booster that caused an increased reaction to Mycobacterium's soluble antigen released by the action of the chemotherapeutic agents. These findings are buttressed by significant increase in IgG class antibody levels after healing. [43] Caplin et al. have also shown higher titres of IgG2 antibody to the whole killed M. tuberculosis and to the ML34 epitope shared by many species of mycobacteria. [44] In consonance with our study, this latter group of workers also found that the severity of TB, defined radiologically, was not related to current features of cell-mediated immunity.

In conclusion, this study demonstrates that there are changes in the T-lymphocyte number and distribution in patients suffering from pulmonary TB. The identification of these changes is a first step. In addition, there is a need to further evaluate the mechanisms leading to these changes so as to understand the pathogenesis and prognostic markers of the disease and to develop immunomodulatory modalities of therapy.

 :: References Top

1.Dye C, Scheele S, Dolin R, Pathania V, Raviglione MC. Consensus Statement. Global burden of tuberculosis: Estimated incidence, prevalence and mortality by country. WHO Global Surveillance and Monitoring Project. JAMA 1999;282:677-86.  Back to cited text no. 1    
2.Selwyn PA, Hartel D, Lewis VA, Schoenbaum EE, Vermund SH, Klein RS, et al . A prospective study of the risk of tuberculosis among intravenous drug users with human deficiency virus infection. N Engl J Med 1989;320:545-50.  Back to cited text no. 2  [PUBMED]  
3.Styblo K. Recent advances in epidemiological research in tuberculosis. Adv Tuberc Res 1980;20:1-63.  Back to cited text no. 3  [PUBMED]  
4.DeCock KM, Chaisson RE. Will DOTs do it? A reappraisal of tuberculosis control I countries with high rates of HIV infection. Int J Tuber Lung Dis 1999;3:457-65.  Back to cited text no. 4    
5.World Health Organization Factsheet No. 104, March 2006.  Back to cited text no. 5    
6.Pablos-Mendez A, Raviglione MC, Laszlo A, Binkin N, Reider HL, Bustreo F, et al . Global surveillance for anti-tuberculous-drug resistance, 1994-1997: World Health Organization International Union against Tuberculosis and Lung Disease Working Group on Anti-Tuberculous Drug Resistance Surveillance. N Engl J Med 1998;338:1641-9.  Back to cited text no. 6    
7.Snider DE Jr, Castro KG. The global threat of drug resistant tuberculosis. N Engl J Med 1998;338:1689-90.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]
8.Hass WD. Mycobacterium tuberculosis . In: Mandell GL, Bennett EJ, Dolin R, editors. Principle and Practice of Infectious Diseases. Churchill Livingstone: Philadelphia; 2000. p. 2582-3.  Back to cited text no. 8    
9.Flynn J, Chan J. Immunology of tuberculosis. Annu Rev Immunol 2001;19:93-130.  Back to cited text no. 9    
10.Orme IM, Collins FM. Protection against Mycobacterium tuberculosis infection by adoptive immunotherapy: Requirement for T cell-deficient recipients. J Exp Med 1983;158:74-83.  Back to cited text no. 10  [PUBMED]  
11.Raja A. Immunology of tuberculosis. Indian J Med Res 2004;120:213-32.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]
12.Kindler V, Sappino AP, Grau GE, Piguet PF, Vassalli P. The inducing role of tumour necrosis factor in the development of bactericidal granulomas during BCG infection. Cell 1989;56:731-40.  Back to cited text no. 12  [PUBMED]  [FULLTEXT]
13.Chackerian A, Alt J, Perera V, Behar SM. Activation of NKT cells protects mice from tuberculosis. Immun Infect 2002;70:6302-9.  Back to cited text no. 13    
14.Godfrey DI, Hammond KJ, Poulton LD, Smyth MJ. NKT cells: Facts, functions and fallacies. Immunol Today 2000;21:573-83.  Back to cited text no. 14    
15.Tollerud DJ, Clark JW, Brown LM, Neuland CY, Mann DL, Pankiw-Trost LK, et al . The influence of age and gender on peripheral blood mononuclear subsets in healthy non-smokers. J Clin Immunol 1989;9:214-22.  Back to cited text no. 15    
16.Shahabuddin S. Quantitative differences in CD8+ lymphocytes, CD4/CD8 ratio, NK cells and HLA-DR+ activated T cells of racially different male populations. Clin Immunol Immunopathol 1995;75:168-70.  Back to cited text no. 16  [PUBMED]  [FULLTEXT]
17.Lee BW, Yap HK, Chew FT, Quah TC, Prabhakarn K, Chan GS, et al . Age and sex related changes in lymphocyte subpopulations in healthy Asian subjects: From birth to childhood. Cytometry 1996;26:8-15.  Back to cited text no. 17    
18.Al Qouzi A, Al Salamah A, Al Rasheed R, Al Mussalam A, Al Khairy K, Kheir O, et al . Immunophenotyping of Peripheral Blood Lymphocytes in Saudi Men. Clin Diag Lab Immunol 2002;9:279-81.  Back to cited text no. 18    
19.Singhal M, Banavalikar JN, Sharma S, Saha K. Peripheral blood T lymphocyte subpopulations in patients with tuberculosis and the effect of chemotherapy. Tubercle 1989;70:171-8.  Back to cited text no. 19  [PUBMED]  
20.Onwubalili JK, Edwards AJ, Palmer L. T4 lymphopenia in human tuberculosis. Tubercle 1987;68:195-200.  Back to cited text no. 20  [PUBMED]  
21.Swaminathan S, Nandini KS, Hanna LE, Somu N, Narayanan PR, Barnes PF. T-lymphocyte subpopulation in tuberculosis. Indian Pediatr 2000;375:489-95.  Back to cited text no. 21    
22.Pithie AD, Rahelu M, Kumararatne DS, Drysdale P, Gaston JS, Iles PB, et al . Generation of cytolytic T cells in individuals infected by Mycobacterium tuberculosis and vaccinated with BCG. Thorax 1992;47:695-701.  Back to cited text no. 22  [PUBMED]  
23.Scanga CA, Mohan VP, Yu K, Joseph H, Tanaka K, Chan J, et al . Depletion of CD4 T cells causes reactivation of murine persistent tuberculosis despite continued expression of interferon gamma and nitric oxide synthase 2. J Exp Med 2000;192:347-58.  Back to cited text no. 23  [PUBMED]  [FULLTEXT]
24.Ordway D, Harton M, Henao-Tamayo M, Orme IM, Gonzalez-Juarrero M. Enhanced macrophage activity in granuloumatous lesions of immune mice challenged with Mycobacterium tuberculosis . J Immunol 2006;176:4931-9.  Back to cited text no. 24  [PUBMED]  [FULLTEXT]
25.Jones BE, Maung M, Takewel EK, Gian D, Kumar A, Maslow ER, et al . CD4 cell count in human immunodeficiency virus negative patients with tuberculosis. Clin Infect Dis 1997;24:988-91.  Back to cited text no. 25    
26.Rodrigues DS, Medeiros EA, Weckx LY, Bonnez W, Salomao R, Kallas EG. Immunophenotypic characterization of peripheral T lymphocytes in Mycobacterium tuberculosis infection and disease. Clin Exp Immunol 2002;128:149-54.  Back to cited text no. 26    
27.Gonzalez-Jaurrero M, Turner OC, Turner J, Maretta P, Brooks JV, Orme IM. Temporal and spatial arrangement of lymphocytes within lung granulomas induced by aerosol infection with Mycobacterium tuberculosis . Infect Immun 2001;69:1722-8.  Back to cited text no. 27    
28.Rook GA, Carswell JW, Stanford JL. Preliminary evidence for the trapping of antigen-specific lymphocytes in the lymphoid tissue of 'anergic' tuberculous patients. Clin Exp Immunol 1976;26:129-32.  Back to cited text no. 28  [PUBMED]  [FULLTEXT]
29.Ainslie GM, Solomon JA, Bateman ED. Lyphocytes and lymphocyte subset numbers in blood and in bronchoalveolar lavage and pleural fluid in various forms of human pulmonary tuberculosis at presentation and during recovery. Thorax 1992;47:513-8.   Back to cited text no. 29  [PUBMED]  
30.Tsao TC, Chen CH, Hong JH, Hsieh MJ, Tsao KC, Lee CH. Shifts of T4/T8 lymphocytes from BAL fluid and peripheral blood by clinical grade in patients with pulmonary tuberculosis. Chest 2002;122:1285-91.  Back to cited text no. 30  [PUBMED]  [FULLTEXT]
31.Tascon RE, Stavropoulos E, Lukacs KV, Colston MJ. Protection against Mycobacterium tuberculosis infection by CD8 T cells requires the production of gamma interferon. Infect Immun 1998;66:830-4.  Back to cited text no. 31  [PUBMED]  [FULLTEXT]
32.Lalvani A, Brookes R, Wilkinson RJ, Malin AS, Pathan AA, Andersen P, et al . Human cytolytic and interferon gamma-secreting CD8 T lymphocytes specific for Mycobacterium tuberculosis . Proc Natl Acad Sci USA 1998;95:270-5.  Back to cited text no. 32  [PUBMED]  [FULLTEXT]
33.Flynn JL, Goldstein MM, Tiebold KJ, Koller B, Bloom BR. Major histocompatibility class 1-restricted T cells are required for resistance to Mycobacterium tuberculosis infection. Proc Natl Acad Sci USA 1992;89:12013-7.   Back to cited text no. 33    
34.Chin SF, Cheong SK, Lim YC, Ton SH. The distribution of immunoregulatory cells in the peripheral blood of normal Malaysian adults. J Pathol 1993;15:49-52.  Back to cited text no. 34    
35.Barcelos W, Martins-Filho OA, Guimaraes TM, Oliveira MH, Spindola-de-Miranda S, Carvlho BN, et al . Peripheral blood mononuclear cells immunophenotyping in pulmonary tuberculosis patients before and after treatment. Microbiol Immunol 2006;50:597-605.  Back to cited text no. 35    
36.Pessaran Z, Sahebfosul F, Oreizi F, Ghavaminejad A, Kiani A, Siadat ZD. Immunophenotypic characterization of peripheral blood T-Lymphocytes and their subpopulations in tuberculosis patients before and after treatments. Iran J Allergy Asthma Immunol 2005;4:23-6.   Back to cited text no. 36    
37.Robertson MJ, Ritz C. Biology and clinical relevance of human natural killer cells. Blood 1990;76:2421-38.  Back to cited text no. 37    
38.Jason J, Buchanan I, Archibald LK, Nwanyanwu OC, Bell M, Grenn AT, et al . Natural T, d and NK cells in mycobacterial, salmonella and human immunodeficiency virus infections. J Infect Dis 2000;182:474-81.  Back to cited text no. 38    
39.Dieli F, Taniguchi M, Kronenberg M, Sidobre S, Ivany J, Fattorini L, et al A anti-inflammatory role for Va14 NK T cells in Mycobacterium bovis Bacillus Calmete-Guerin-Infected mice. J Immunol 2003;171:1961-8.  Back to cited text no. 39    
40.Kadowaki N, Antonenko S, Ho S, Rissoan MC, Soumelis V, Porcelli SA, et al . Distinct cytokine profiles of neonatal natural killer T cells after expansion with subsets of dendritic cells. J Exp Med 2001;10:1221-6.  Back to cited text no. 40    
41.Dalbeth N, Gundle R, Davies J, Lee CG, McMichael AJ, Callan FC. CD56bright NK cells are enriched at inflammatory sites and can engage with monocytes in a reciprocal program of activation. J Immunol 2004;173:6418-26.  Back to cited text no. 41    
42.Cooper MA, Turner CS, Chen KS, Ghaheri AB, Ghayur T, Carson WE, et al . Human natural killer cells: A unique innate immunoregulatory role for the CD56bright subset. Immunology 2001;15:3146-51.  Back to cited text no. 42    
43.Dubaniewicz A, Sztaba-Kania M, Hoppe A. Analysis of some immunological parameters in pulmonary tuberculosis. Pol Merkuriusz Lek 2004;16:123-7.  Back to cited text no. 43    
44.Caplin M, Grange JM, Morley S, Brown RA, Kemp M, Gibson JA, et al . Relationship between radiological classification and the serological and haematological features of untreated pulmonary tuberculosis in Indonesia. Tubercle 1989;70:103-13.  Back to cited text no. 44  [PUBMED]  


  [Table - 1], [Table - 2], [Table - 3]

This article has been cited by
1 Invariant Natural Killer T Cells: Boon or Bane in Immunity to Intracellular Bacterial Infections?
Sudhanshu Shekhar, Antony George Joyee, Xi Yang
Journal of Innate Immunity. 2014; 6(5): 575
[Pubmed] | [DOI]
2 Lymphocyte subgroups in different forms of tuberculosis [Farkli{dotless
Aksu, K. and Kurt, E. and Parspour, S. and Orman, A. and Glbaş, Z.
Turk Toraks Dergisi. 2012; 13(1): 1-5
3 Association of immunophenotypic characterization of peripheral lymphocytes with different clinical phenotypes of tuberculosis in Chinese Han children
Xiao, J. and Sun, L. and Wu, X. and Miao, Q. and Jiao, W. and Shen, C. and Shen, D. and Feng, W. and Liu, F. and Shen, A.
Chinese Medical Journal. 2012; 125(2): 275-280
4 Immunohistochemical evaluation of surfactant proteins and lymphocyte phenotypes in the lungs of cattle with natural tuberculosis
Enver Beytut
Research in Veterinary Science. 2011; 91(1): 119
[VIEW] | [DOI]
5 Significant increase in natural-killer T cells in patients with tuberculosis complicated by type 2 diabetes mellitus
Zhang, Q., Xiao, H-P., Cui, H-Y., Sugawara, I.
Journal of International Medical Research. 2011; 39(1): 105-111
6 Inhibitory Function of Interferon on Hepatocarcinogenesis
Hirohisa Yano
Oncology. 2008; 75(Suppl. 1): 22
[Pubmed] | [DOI]


Print this article  Email this article
Previous article Next article
Online since 12th February '04
2004 - Journal of Postgraduate Medicine
Official Publication of the Staff Society of the Seth GS Medical College and KEM Hospital, Mumbai, India
Published by Wolters Kluwer - Medknow