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Review
. 2022 Jan-Dec:36:3946320221078436.
doi: 10.1177/03946320221078436.

Immune response against toxoplasmosis-some recent updates RH: Toxoplasma gondii immune response

Madiha Sana  1 , Muhammad Rashid  2 , Imran Rashid  1 , Haroon Akbar  1 , Jorge E Gomez-Marin  3 , Isabelle Dimier-Poisson  4
Affiliations
Review

Immune response against toxoplasmosis-some recent updates RH: Toxoplasma gondii immune response

Madiha Sana et al. Int J Immunopathol Pharmacol. 2022 Jan-Dec.

Abstract

Aims: Cytokines, soluble mediators of immunity, are key factors of the innate and adaptive immune system. They are secreted from and interact with various types of immune cells to manipulate host body's immune cell physiology for a counter-attack on the foreign body. A study was designed to explore the mechanism of Toxoplasma gondii (T. gondii) resistance from host immune response.

Methods and results: The published data on aspect of host (murine and human) immune response against T. gondii was taken from Google scholar and PubMed. Most relevant literature was included in this study. The basic mechanism of immune response starts from the interactions of antigens with host immune cells to trigger the production of cytokines (pro-inflammatory and anti-inflammatory) which then act by forming a cytokinome (network of cytokine). Their secretory equilibrium is essential for endowing resistance to the host against infectious diseases, particularly toxoplasmosis. A narrow balance lying between Th1, Th2, and Th17 cytokines (as demonstrated until now) is essential for the development of resistance against T. gondii as well as for the survival of host. Excessive production of pro-inflammatory cytokines leads to tissue damage resulting in the production of anti-inflammatory cytokines which enhances the proliferation of Toxoplasma. Stress and other infectious diseases (human immunodeficiency virus (HIV)) that weaken the host immunity particularly the cellular component, make the host susceptible to toxoplasmosis especially in pregnant women.

Conclusion: The current review findings state that in vitro harvesting of IL12 from DCs, Np and MΦ upon exposure with T. gondii might be a source for therapeutic use in toxoplasmosis. Current review also suggests that therapeutic interventions leading to up-regulation/supplementation of SOCS-3, IL12, and IFNγ to the infected host could be a solution to sterile immunity against T. gondii infection. This would be of interest particularly in patients passing through immunosuppression owing to any reason like the ones receiving anti-cancer therapy, the ones undergoing immunosuppressive therapy for graft/transplantation, the ones suffering from immunodeficiency virus (HIV) or having AIDS. Another imortant suggestion is to launch the efforts for a vaccine based on GRA6Nt or other similar antigens of T. gondii as a probable tool to destroy tissue cysts.

Keywords: Toxoplasma gondii; cytokinomes; host immune response; host resistance; susceptibility.

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Conflict of interest statement

Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Figures

Figure 1.
Figure 1.
Outcome of toxoplasmosis in case of resistance and susceptibility.
Figure 2.
Figure 2.
Pathways for host susceptibility and resistance in human Toxoplasmosis, particularly as a result of IL6.
See this image and copyright information in PMC

References

    1. Chen XQ, Zhou CX, Elsheikha HM, et al. (2017) Profiling of the perturbed metabolomic state of mouse spleen during acute and chronic toxoplasmosis. Parasites Vectors 10(1): 339. - PMC - PubMed
    1. White MW, Radke JR, Radke JB. (2014) Toxoplasma development - turn the switch on or off? Cell Microbiol 16(4): 466–472. - PubMed
    1. Fisch D, Clough B, Frickel E-M. (2019) Human immunity to Toxoplasma gondii. PLoS Pathogens 15(12): e1008097. - PMC - PubMed
    1. Costantini S, Castello G, Colonna G. (2010) Human Cytokinome: a new challenge for systems biology. Bioinformation 5(4): 166–167. - PMC - PubMed
    1. Sarciron M, Gherardi A. (2000) Cytokines involved in Toxoplasmic encephalitis. Scand J Immunol 52(6): 534–543. - PubMed