Batf2 differentially regulates tissue immunopathology in Type 1 and Type 2 diseases. Guler, R., Mpotje, T., Ozturk, M., Nono, J. K, Parihar, S. P, Chia, J. E., Abdel Aziz, N., Hlaka, L., Kumar, S., Roy, S., Penn-Nicholson, A., Hanekom, W. A, Zak, D. E, Scriba, T. J, Suzuki, H., & Brombacher, F. Mucosal Immunology, 12:390–402, Nature Publishing Group, dec, 2019. ![Batf2 differentially regulates tissue immunopathology in Type 1 and Type 2 diseases [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex Basic leucine zipper transcription factor 2 (Batf2) activation is detrimental in Type 1-controlled infectious diseases, demonstrated during infection with Mycobacterium tuberculosis (Mtb) and Listeria monocytogenes Lm. In Batf2-deficient mice (Batf2−/−), infected with Mtb or Lm, mice survived and displayed reduced tissue pathology compared to infected control mice. Indeed, pulmonary inflammatory macrophage recruitment, pro-inflammatory cytokines and immune effectors were also decreased during tuberculosis. This explains that batf2 mRNA predictive early biomarker found in active TB patients is increased in peripheral blood. Similarly, Lm infection in human macrophages and mouse spleen and liver also increased Batf2 expression. In striking contrast, Type 2-controlled schistosomiasis exacerbates during infected Batf2−/− mice with increased intestinal fibro-granulomatous inflammation, pro-fibrotic immune cells, and elevated cytokine production leading to wasting disease and early death. Together, these data strongly indicate that Batf2 differentially regulates Type 1 and Type 2 immunity in infectious diseases.
@article{Guler2018,
abstract = {Basic leucine zipper transcription factor 2 (Batf2) activation is detrimental in Type 1-controlled infectious diseases, demonstrated during infection with Mycobacterium tuberculosis (Mtb) and Listeria monocytogenes Lm. In Batf2-deficient mice (Batf2−/−), infected with Mtb or Lm, mice survived and displayed reduced tissue pathology compared to infected control mice. Indeed, pulmonary inflammatory macrophage recruitment, pro-inflammatory cytokines and immune effectors were also decreased during tuberculosis. This explains that batf2 mRNA predictive early biomarker found in active TB patients is increased in peripheral blood. Similarly, Lm infection in human macrophages and mouse spleen and liver also increased Batf2 expression. In striking contrast, Type 2-controlled schistosomiasis exacerbates during infected Batf2−/− mice with increased intestinal fibro-granulomatous inflammation, pro-fibrotic immune cells, and elevated cytokine production leading to wasting disease and early death. Together, these data strongly indicate that Batf2 differentially regulates Type 1 and Type 2 immunity in infectious diseases.},
author = {Guler, Reto and Mpotje, Thabo and Ozturk, Mumin and Nono, Justin K and Parihar, Suraj P and Chia, Julius Ebua and {Abdel Aziz}, Nada and Hlaka, Lerato and Kumar, Santosh and Roy, Sugata and Penn-Nicholson, Adam and Hanekom, Willem A and Zak, Daniel E and Scriba, Thomas J and Suzuki, Harukazu and Brombacher, Frank},
doi = {10.1038/s41385-018-0108-2},
file = {:C$\backslash$:/Users/01462563/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/Guler et al. - 2019 - Batf2 differentially regulates tissue immunopathology in Type 1 and Type 2 diseases.pdf:pdf},
journal = {Mucosal Immunology},
keywords = {OA,fund{\_}ack,original},
mendeley-tags = {OA,fund{\_}ack,original},
month = {dec},
pages = {390--402},
pmid = {30542107},
publisher = {Nature Publishing Group},
title = {{Batf2 differentially regulates tissue immunopathology in Type 1 and Type 2 diseases}},
url = {http://www.nature.com/articles/s41385-018-0108-2},
volume = {12},
year = {2019}
}
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This explains that batf2 mRNA predictive early biomarker found in active TB patients is increased in peripheral blood. Similarly, Lm infection in human macrophages and mouse spleen and liver also increased Batf2 expression. In striking contrast, Type 2-controlled schistosomiasis exacerbates during infected Batf2−/− mice with increased intestinal fibro-granulomatous inflammation, pro-fibrotic immune cells, and elevated cytokine production leading to wasting disease and early death. 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