Lymphocyte Subset Variations in Pulmonary Tuberculosis
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Annals of Experimental Biology

Commentary - Annals of Experimental Biology ( 2022) Volume 10, Issue 6

Lymphocyte Subset Variations in Pulmonary Tuberculosis

Alice Brown*
Editorial Office, Annals of Experimental Biology, Uxbridge, United Kingdom
*Corresponding Author:
Alice Brown, Editorial Office, Annals of Experimental Biology, Uxbridge, United Kingdom, Email: info@scholarsresearchlibrary

Received: 10-Nov-2022, Manuscript No. AEB-22-84440; Editor assigned: 12-Nov-2022, Pre QC No. AEB-22-84440 (PQ); Reviewed: 22-Nov-2022, QC No. AEB-22-84440 (Q); Revised: 24-Nov-2022, Manuscript No. AEB-22-84440 (R); Published: 29-Nov-2022 , DOI: 0


The pathogenesis and defensive mechanisms of Mycobacterium tuberculosis depend heavily on the human immune system (Mtb). This investigation looked at how people with Pulmonary Tuberculosis (PTB) changed their immune systems. In PTB patients, the immune system’s outward signs were altered; the infection’s inflammatory response was constrained, which reduced innate immune activation, and an increase in T and B cell responses served as the primary means of pathogen eradication.


Lymphocyte, Pulmonary Tuberculosis


Mycobacterium tuberculosis is the culprit behind Pulmonary Tuberculosis (PTB) (Mtb). Sputum smear acid-fast staining test, Mtb in sputum culture, and Genexpert detection technology are the three primary techniques of bacteriological testing, which can assist in confirming the diagnosis of PTB. Although tuberculosis research has been ongoing for a long time, the pathophysiology is still not entirely understood. This study was created in order to further investigate the changes in immune responses in PTB patients because host immunological status is a significant factor affecting the outcome after Mtb infection.

A parasitic bacteria, Mtb. The pathogenesis and defensive mechanisms of Mtb are significantly influenced by the host immune system, and cell-mediated immunity is the primary immunological response (CMI). The Mtb strains have been found to promote CD4+ T cell proliferation. Following infection, Mtb first stimulates the body’s innate defenses before being recognized by natural receptors on the surface of macrophages, which subsequently release phagolysosomes to destroy the bacterium. Patient’s peripheral blood levels of CD4 + T cells rise as a result of this process, which raises the ratio of CD4+/CD8 + T cells and causes immune system abnormalities that hasten the development of the disease. B cells’ contribution to immunity against PTB is still debatable. According to several researchers, the majority of investigations on individuals with PTB looked at B cells isolated from peripheral blood rather than inflamed Mtb-affected tissues, which produced conflicting results on B cell numbers in PTB. Experimental findings demonstrated the occurrence of inhibitory anti-PstS1 B cell responses during active TB.

The primary innate immune effector cells are NK cells, which have strong cytolytic abilities without MHC restriction. Following Mtb attachment to the NKp44 Natural Cytotoxicity Receptor (NCR) on NK cells, the cells can either directly or indirectly regulate mycobacterial development by activating macrophages and using cytotoxic processes

The amount of CRP is regarded as an acute clinical signal, and it frequently correlates with the severity of the illness. In comparison to bacterial pneumonia, PTB had a lower median CRP, according to a prior study.

PTB is frequently mistaken for other lung conditions. The prevalence and virulence of the bacteria, human immunity, and other elements all affect how the disease develops. This study showed that the immune system’s appearance in PTB was distinct from that in healthy individuals and CAP, that the infection’s inflammation was constrained, reducing innate immune activation, and that an increase in T and B cell responses served as the primary pathogen-elimination strategy.