T FOLLICULAR REGULATORY CELLS CONTROL THE IGE RESPONSE

Authors

  • Axmedova D.K. Department of Phthisiatry and Pulmonology, Microbiology, Virology, and Immunology Assistant Andijan State Medical Institute.

Keywords:

Allergic airway inflammation,food allergy, IgE,T follicular regulatory cells

Abstract

One of the main mediators of allergic reactions and a primary cause of allergy illness in humans is allergen-specific IgE. It would be beneficial to reduce the prevalence of allergic illness by using therapies that block the formation of IgE. The regulation of IgE reactions has been the subject of extensive study, and a number of variables that encourage the synthesis of allergic IgE have been identified. The formation of IgE-producing B cells in the germinal center (GC) depends on T follicular helper (TFH) cells expressing IL-4. Anaphylaxis, a strong allergic reaction, is encouraged by high affinity allergen-specific IgE that is developed as a result of Ig somatic hypermutation and B cell selection in the GC. In the GC response, T follicular regulatory (TFR) cells are also present. They collaborate with TFH cells to select high affinity IgE + B cells. The literature on TFR cells and IgE reactions is reviewed in this study. TFR cells have been shown in animal studies to have a suppressive effect on IgE responses in allergic airway illness; yet, they also assist in the IgE response in food allergies. TFR cells have been linked in human studies to a reduced allergic reaction; nevertheless, there is insufficient data to support a direct suppressive function of TFR cells on IgE in vivo. TFR cells might be a novel target for allergy treatments, however care must be taken to encourage TFR cells' suppressor rather than their helper functions.\

References

M.I. Asher, S. Montefort, B. Bjorksten, C.K. Lai, D.P. Strachan, S.K. Weiland, et al. Worldwide time trends in the prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and eczema in childhood: ISAAC Phases One and Three repeat multicountry cross-sectional surveys Lancet, 368 (2006), pp. 733-743

S.H. Sicherer, H.A. Sampson Peanut allergy: emerging concepts and approaches for an apparent epidemic J Allergy Clin Immunol, 120 (2007), pp. 491-503

M. Dullaers, R. De Bruyne, F. Ramadani, H.J. Gould, P. Gevaert, B.N. Lambrecht The who, where, and when of IgE in allergic airway disease J Allergy Clin Immunol, 129 (2012), pp. 635-645

H.J. Gould, B.J. Sutton, A.J. Beavil, R.L. Beavil, N. McCloskey, H.A. Coker, et al. The biology of IGE and the basis of allergic disease Annu Rev Immunol, 21 (2003), pp. 579-628

M. Kopf, G. Le Gros, M. Bachmann, M.C. Lamers, H. Bluethmann, G. Kohler Disruption of the murine IL-4 gene blocks Th2 cytokine responses Nature, 362 (1993), pp. 245-248

F.D. Finkelman, I.M. Katona, J.F. Urban Jr., J. Holmes, J. Ohara, A.S. Tung, et al. IL-4 is required to generate and sustain in vivo IgE responses J Immunol, 141 (1988), pp. 2335-2341

Z. Yang, C.M. Wu, S. Targ, C.D.C. Allen IL-21 is a broad negative regulator of IgE class switch recombination in mouse and human B cells J Exp Med, 217 (2020), Article e20190472

O. Talay, D. Yan, H.D. Brightbill, E.E. Straney, M. Zhou, E. Ladi, et al. IgE(+) memory B cells and plasma cells generated through a germinal-center pathway Nat Immunol, 13 (2012), pp. 396-404

Published

2024-09-25

How to Cite

Axmedova D.K. (2024). T FOLLICULAR REGULATORY CELLS CONTROL THE IGE RESPONSE. Ethiopian International Journal of Multidisciplinary Research, 11(09), 137–139. Retrieved from https://www.eijmr.org/index.php/eijmr/article/view/1948