Tuberculosis IgG ELISA Kit

Tuberculosis (TB) is a bacteria disease caused by the Mycobacterium tuberculosis (Mtb) which usually starts in the lungs but can progress to other organs. TB kills millions of people a year, says the World Health Organization. Mtb infections are mainly aerosolized to the respiratory system, and then the lungs. Alveolar macrophages also have innate immunity, by detecting the Mtb cell wall and lipids using a number of PRRs such as Toll-like receptors (TLRs) and NOD-like receptors (NLRs). Upon activation of these receptors, cytokines (TNF, IL-1, IFN-) are secreted to trigger local inflammation and prevent the spread of infection's own inbuilt immune system may restrict Mtb's growth, but it has strong immune defences against evasion. It can also stifle macrophage phagocytosis, avoid lysosomal breakdown, and boost its longevity in the host through inhibition of macrophage cytokine production. Mtb largely restrains its replication in the host by the development of granulomas. A granuloma is an immune body, populated by multiple immune cells (including macrophages, T cells and neutrophils) at the site of infection. In granulomas, the key component is the macrophage. They then activate and not only destroy Mtb, they also release cytokines (e.g., TNF) to recruit other immune cells into an immune cluster. This link between macrophages and T cells is essential to Mtb progression. Macrophages deliver Mtb antigens via MHC class II molecules to CD4+ T cells. The T cells that are activated release cytokines like IFN-, further increasing macrophages' antimicrobial capacity. But sometimes Mtb escapes host immune monitoring by altering the shape of macrophages or the form of granulomas.

Figure 1. Primary Pulmonary Tuberculosis in Adults (Source: Lyon SM, et al., 2017)

Adaptive immune responses are principally delivered by T and B cells. CD4+ T cells are pivotal in the Mtb defense. Mtb-specific T cells get excited early in infection and release massive doses of IFN- to drive macrophages and other immune cells into activation, triggering local immune response. Meanwhile, Mtb also engages in intricate immune evasion strategies that prevent the immune system from completely eliminating the pathogen. These mechanisms include the inhibition of macrophage phagocytosis through lipids in the bacterial cell wall, and the suppression of cytokine production (TNF) to avoid lysosome degradation. Mtb can also hijack the activity of host immune cells, turn down T-cell activation, or induce T-cell tolerance, thereby diminishing the immune system's capacity to eliminate Mtb. We are learning to recognize B cells in this role, even if previous work has focused more on T cell responses. When B cells are infected with Mtb, they manage immunity through the production of antibodies. The antibodies can not only induce phagocytosis to eliminate the organism, but also increase macrophage and other immune cell killing of Mtb via antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC). But even as it triggers certain antibody responses, it is still questionable whether antibodies can protect against TB. In most TB patients, antibody levels are very low, and this varies with the number of bacteria and degree of disease. Others report antibodies might modulate latent TB infection, but T cells are still the major immune defense mechanism in diseased TB.

Mtb antibiotic resistance, particularly multidrug-resistant TB (MDR-TB) and extensively drug-resistant TB (XDR-TB), is a threat to TB prevention and control across the world. Mtb builds antibiotic resistance in many ways, from compromising cell walls to producing -lactamases and changing target proteins. Moreover, Mtb also sneaks past the host immune system by way of immune escape pathways, inhibiting proper pathogen clearance. Evidence suggests that immune evasion and antibiotic resistance are coordinated to ensure that Mtb survives in the host and becomes chronically infected. Today, Mtb infection is diagnosed mostly using the tuberculin skin test (TST) and interferon-gamma release assays (IGRA). The TST quantifies the T cell response to Mtb-specific antigens, and IGRA tracks the IFN- produced in the presence of those antigens. These immune diagnostic techniques are especially helpful in the diagnosis of latent TB infection (LTBI). TB treatment mostly consists of anti-TB drugs, including isoniazid and rifampin. But the advent of drug-resistant strains of TB complicates standard treatment protocols. New treatments include a combination of several anti-TB medications, immunotherapy, and vaccination. We continue to explore immunotherapy, including the development of the host immune system to better attack Mtb. BCG, the only available TB vaccine, is not effective in adolescents or adults, but it remains a common method for TB prevention, especially among children.

Figure 2. Role of Antibodies in Mycobacterium tuberculosis Infection (Source: Scriba TJ, et al., 2017)

TB IgG Detection Kit
Mycobacterium tuberculosis IgG ELISA Kit
Anti-Tuberculosis IgG Test Kit
Tuberculosis IgG Antibody Detection Kit