[Download] ~ Does Leptin have a Role in Immunity to Tuberculosis? (Commentary) (Report) # by Indian Journal of Medical Research ~ Book PDF Kindle ePub Free
eBook details
- Title: Does Leptin have a Role in Immunity to Tuberculosis? (Commentary) (Report)
- Author : Indian Journal of Medical Research
- Release Date : January 01, 2008
- Genre: Life Sciences,Books,Science & Nature,Health, Mind & Body,Health & Fitness,
- Pages : * pages
- Size : 65 KB
Description
Tuberculosis infection is acquired through inhalation of aerosolized infectious particles containing Mycobacterium tuberculosis, which can reach the alveoli in the distal airways. Macrophages and dendritic cells (DCs), the first host cells targeted by invading bacilli, are the key mediators of innate immunity to M. tuberculosis. In the course of infection, additional macrophages and resident DCs are recruited to the site of infection. Mature DCs relocate to the lymph nodes where they produce inflammatory cytokines and there is development of adaptive immune response which includes helper (CD4+) T-cells, cytotoxic (CD8+) T-cells, [gamma][delta] T-cells and the production of interferon [gamma] (IFN[gamma]) and tumour necrosis factor [alpha] (TNF[alpha]), both key cytokines in immunity to tuberculosis. The host immune responses sufficiently contain the infection in about 90 per cent of the HIV-negative individuals, without achieving sterilization, and only about 10 per cent of the infected individuals progress to disease. The progression of primary infection to disease is slow in humans taking a few weeks to several years. Chemotherapeutic treatment of clinical disease does not always lead to sterilization. Dormant tubercle bacilli can remain alive within the human host for decades and the bacillary reactivation is kept in check by the host immune response. It has been shown that many cases of tuberculosis result from reactivation of latent infection, at least in countries with low or moderate tuberculosis endemicity (1). Since it is only a small proportion of infected individuals who develop clinical disease, the risk of becoming infected with M. tuberculosis would be different from the risk of progression to active disease, either as progression of primary infection to primary progressive disease or reactivation of latent infection. The rising incidence of tuberculosis over the last two decades has increased the need to define host factors that control resistance to the development of active tuberculosis. Worldwide malnutrition and starvation are major causes of immunosuppression and increased susceptibility to tuberculosis (2). Several different aspects of malnutrition can be held responsible for the immunosuppression, and recently leptin has been described as a possible link between nutrition and immune status. Leptin, a 16-kDa non-glycosylated polypeptide protein is produced mainly by the adipocytes, and the circulating concentrations are proportional to fat mass (3). By virtue of its structural similarity to the type I cytokine superfamily (4), and the expression of its functional receptor in all cell types of innate and adaptive immunity, leptin is shown to modulate the immune response and favour a Th1 response while inhibiting the secretion of Th2 cytokines (5,6). Leptin signaling has been shown to promote the maturation of DCs, activation of monocytes, macrophages and natural killer cells (7-9). In the absence of leptin signaling, DCs display a Th2biased cytokine profile, and altered Th1:Th2 cytokine balance is associated with a corresponding change in the immuno-stimulatory capacity on T cells (7,8). Furthermore, leptin is shown to promote the survival of DCs, T and B lymphocytes by suppressing Fas-mediated apoptosis, which may result from its induction of anti-apoptotic proteins and downregulation of pro-apoptotic proteins (8,10). Recently it has also been shown that leptin can act as a negative signal for the proliferation of Foxp3+ regulatory T cells. Regulatory T cells have been shown to suppress Th1 immune responses (11). Thus reduced leptin concentrations by virtue of impairment of Th1 cell-mediated immunity may present a risk factor for development of tuberculosis. Indeed it has been shown that leptin-deficient mice are more susceptible to M. tuberculosis than wild-type mice, suggesting that leptin contributes to protection against tuberculosis (12). Similarly low serum leptin level associated with reduced body f
 (Report) # by Indian Journal of Medical Research ~ Book PDF Kindle ePub Free){kind=link}
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