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Immunity against Mycobacterium tuberculosis and the risk of biologic anti-TNF-α reagents.

Yasui K - Pediatr Rheumatol Online J (2014)

Bottom Line: Recently, it is well established that innate immunity as well plays a definitive role in the development of TB immunity under the effects of several cytokines, microbicidal proteins and Toll-like receptors.Meanwhile, the introduction and widespread use of biological disease-modifying anti-rheumatic reagents over the last 15 years worldwide has dramatically advanced and improved the standard care and prognosis of patients with rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA).The knowledge of basic immunology has also advanced over the past 10 years and adult and pediatric rheumatologists should increase their understanding of this dynamic between arthritis diseases, anti-TNF-α medications, and TB.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, Hiroshima-City Hospital, Moto-Machi 7-33, Naka-Ku Hiroshima, 730-8518 Japan ; Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.

ABSTRACT
A third of the world's population is exposed to Mycobacterium tuberculosis in their lifetime. Over eight million people develop a tuberculosis (TB) illness and 1.3 million people die from the disease every year. Acquired immunity (cytotoxic CD8+ T cells (CBT), Th1 CD4+ helper T cells) macrophages, and dendritic cells all play important roles in TB infection. Recently, it is well established that innate immunity as well plays a definitive role in the development of TB immunity under the effects of several cytokines, microbicidal proteins and Toll-like receptors. Meanwhile, the introduction and widespread use of biological disease-modifying anti-rheumatic reagents over the last 15 years worldwide has dramatically advanced and improved the standard care and prognosis of patients with rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA). However, as clinical experience with these drugs has grown, the risk of granulomatous infections, especially disseminated TB and fungal infections, has become apparent, especially because having RA or JIA may innately increase the risk of infection (bacterial, viral and fungal). The knowledge of basic immunology has also advanced over the past 10 years and adult and pediatric rheumatologists should increase their understanding of this dynamic between arthritis diseases, anti-TNF-α medications, and TB. This review will provide an up-to-date discussion of both the immunology of the TB organism in the human host and the pathophysiologic mechanisms of the TNF-α blockers in the development of secondary (disseminated) tuberculosis.

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Related in: MedlinePlus

Key functions of the tumor necrosis factor (TNF)-α cytokine in tuberculosis. (A) TNF-α recruits neutrophils, macrophages and T-lymphocytes to the infection site; (B) The cytokine maintains granuloma formation in tuberculosis; (C) The autocrinal TNF-α is also produced and induces apoptosis of TB-infected cells.
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Fig5: Key functions of the tumor necrosis factor (TNF)-α cytokine in tuberculosis. (A) TNF-α recruits neutrophils, macrophages and T-lymphocytes to the infection site; (B) The cytokine maintains granuloma formation in tuberculosis; (C) The autocrinal TNF-α is also produced and induces apoptosis of TB-infected cells.

Mentions: Granuloma formation can prevent infectious expansion (dissemination). Langhans giant cells, lymphocytes, fibroblast cells surround the ingested TB bacteria [3, 18, 25] and in the presence of TNF-α, a granuloma is then effectively formed (Figures 4 and 5). The TB bacillus is captured in a granuloma but can survive inside [26]. The space is replaced by the caseation organization, and in most cases, the TB bacillus remains in a dormant state (latent infection). Caseation organization is exaggerated in the presence of TNF-α.Figure 4


Immunity against Mycobacterium tuberculosis and the risk of biologic anti-TNF-α reagents.

Yasui K - Pediatr Rheumatol Online J (2014)

Key functions of the tumor necrosis factor (TNF)-α cytokine in tuberculosis. (A) TNF-α recruits neutrophils, macrophages and T-lymphocytes to the infection site; (B) The cytokine maintains granuloma formation in tuberculosis; (C) The autocrinal TNF-α is also produced and induces apoptosis of TB-infected cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4196001&req=5

Fig5: Key functions of the tumor necrosis factor (TNF)-α cytokine in tuberculosis. (A) TNF-α recruits neutrophils, macrophages and T-lymphocytes to the infection site; (B) The cytokine maintains granuloma formation in tuberculosis; (C) The autocrinal TNF-α is also produced and induces apoptosis of TB-infected cells.
Mentions: Granuloma formation can prevent infectious expansion (dissemination). Langhans giant cells, lymphocytes, fibroblast cells surround the ingested TB bacteria [3, 18, 25] and in the presence of TNF-α, a granuloma is then effectively formed (Figures 4 and 5). The TB bacillus is captured in a granuloma but can survive inside [26]. The space is replaced by the caseation organization, and in most cases, the TB bacillus remains in a dormant state (latent infection). Caseation organization is exaggerated in the presence of TNF-α.Figure 4

Bottom Line: Recently, it is well established that innate immunity as well plays a definitive role in the development of TB immunity under the effects of several cytokines, microbicidal proteins and Toll-like receptors.Meanwhile, the introduction and widespread use of biological disease-modifying anti-rheumatic reagents over the last 15 years worldwide has dramatically advanced and improved the standard care and prognosis of patients with rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA).The knowledge of basic immunology has also advanced over the past 10 years and adult and pediatric rheumatologists should increase their understanding of this dynamic between arthritis diseases, anti-TNF-α medications, and TB.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, Hiroshima-City Hospital, Moto-Machi 7-33, Naka-Ku Hiroshima, 730-8518 Japan ; Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.

ABSTRACT
A third of the world's population is exposed to Mycobacterium tuberculosis in their lifetime. Over eight million people develop a tuberculosis (TB) illness and 1.3 million people die from the disease every year. Acquired immunity (cytotoxic CD8+ T cells (CBT), Th1 CD4+ helper T cells) macrophages, and dendritic cells all play important roles in TB infection. Recently, it is well established that innate immunity as well plays a definitive role in the development of TB immunity under the effects of several cytokines, microbicidal proteins and Toll-like receptors. Meanwhile, the introduction and widespread use of biological disease-modifying anti-rheumatic reagents over the last 15 years worldwide has dramatically advanced and improved the standard care and prognosis of patients with rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA). However, as clinical experience with these drugs has grown, the risk of granulomatous infections, especially disseminated TB and fungal infections, has become apparent, especially because having RA or JIA may innately increase the risk of infection (bacterial, viral and fungal). The knowledge of basic immunology has also advanced over the past 10 years and adult and pediatric rheumatologists should increase their understanding of this dynamic between arthritis diseases, anti-TNF-α medications, and TB. This review will provide an up-to-date discussion of both the immunology of the TB organism in the human host and the pathophysiologic mechanisms of the TNF-α blockers in the development of secondary (disseminated) tuberculosis.

Show MeSH
Related in: MedlinePlus