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A mathematical model for cellular immunology of tuberculosis

  • Received: 01 February 2010 Accepted: 29 June 2018 Published: 01 August 2011
  • MSC : Primary: 34D23, 93D20; Secondary: 65L05.

  • Tuberculosis (TB) is a global emergency. The World Health Organization reports about 9.2 million new infections each year, with an average of 1.7 million people killed by the disease. The causative agent is Mycobacterium tuberculosis (Mtb), whose main target are the macrophages, important immune system cells. Macrophages and T cell populations are the main responsible for fighting the pathogen. A better understanding of the interaction between Mtb, macrophages and T cells will contribute to the design of strategies to control TB. The purpose of this study is to evaluate the impact of the response of T cells and macrophages in the control of Mtb. To this end, we propose a system of ordinary differential equations to model the interaction among non-infected macrophages, infected macrophages, T cells and Mtb bacilli. Model analysis reveals the existence of two equilibrium states, infection-free equilibrium and the endemically infected equilibrium which can represent a state of latent or active infection, depending on the amount of bacteria.

    Citation: Eduardo Ibarguen-Mondragon, Lourdes Esteva, Leslie Chávez-Galán. A mathematical model for cellular immunology of tuberculosis[J]. Mathematical Biosciences and Engineering, 2011, 8(4): 973-986. doi: 10.3934/mbe.2011.8.973

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  • Tuberculosis (TB) is a global emergency. The World Health Organization reports about 9.2 million new infections each year, with an average of 1.7 million people killed by the disease. The causative agent is Mycobacterium tuberculosis (Mtb), whose main target are the macrophages, important immune system cells. Macrophages and T cell populations are the main responsible for fighting the pathogen. A better understanding of the interaction between Mtb, macrophages and T cells will contribute to the design of strategies to control TB. The purpose of this study is to evaluate the impact of the response of T cells and macrophages in the control of Mtb. To this end, we propose a system of ordinary differential equations to model the interaction among non-infected macrophages, infected macrophages, T cells and Mtb bacilli. Model analysis reveals the existence of two equilibrium states, infection-free equilibrium and the endemically infected equilibrium which can represent a state of latent or active infection, depending on the amount of bacteria.


  • This article has been cited by:

    1. Ruiqing Shi, Yang Li, Sanyi Tang, A MATHEMATICAL MODEL WITH OPTIMAL CONTROLS FOR CELLULAR IMMUNOLOGY OF TUBERCULOSIS, 2014, 18, 1027-5487, 10.11650/tjm.18.2014.3739
    2. Priyanka Baloni, Soma Ghosh, Nagasuma Chandra, 2015, Chapter 8, 978-94-017-9513-5, 151, 10.1007/978-94-017-9514-2_8
    3. Edith Mariela Burbano-Rosero, Lourdes Esteva, Eduardo Ibargüen-Mondragón, Mathematical model for the growth of Mycobacterium tuberculosis in the granuloma, 2017, 15, 1551-0018, 407, 10.3934/mbe.2018018
    4. Eduardo Ibargüen-Mondragón, Jhoana P. Romero-Leiton, Lourdes Esteva, Miller Cerón Gómez, Sandra P. Hidalgo-Bonilla, Stability and periodic solutions for a model of bacterial resistance to antibiotics caused by mutations and plasmids, 2019, 76, 0307904X, 238, 10.1016/j.apm.2019.06.017
    5. Hui Cao, Jianquan Li, Pei Yu, Study of immune response in a latent tuberculosis infection model, 2025, 140, 10075704, 108404, 10.1016/j.cnsns.2024.108404
    6. Eduardo Ibargüen-Mondragón, M. Victoria Otero-Espinar, Miller Cerón Gómez, A within-host model on the interaction dynamics between innate immune cells and Mycobacterium tuberculosis, 2025, 22, 1551-0018, 511, 10.3934/mbe.2025019
    7. Mario Fuest, Johannes Lankeit, Masaaki Mizukami, Global solvability of a model for tuberculosis granuloma formation, 2025, 85, 14681218, 104369, 10.1016/j.nonrwa.2025.104369
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  • © 2011 the Author(s), licensee AIMS Press. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0)
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