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Immunology Learning Strategies

Question:

Given the growing mass information on Immunology, what learning strategies do you recommend?

Answer:

By Juan Carlos Aldave Becerra

I recommend 2 learning strategies that have been very useful for me:

1. Find clinical applications, especially if you care for patients with the problem or disease.

For example, when learning about immune tolerance and T regulatory cells:

  • T regulatory immunity is essential to prevent the development of allergies and autoimmune diseases.
  • Individuals with a reduced number or function of regulatory T lymphocytes are at increased risk of autoimmunity and allergies. For example, patients with pathogenic mutations in the FOXP3 gene develop IPEX (immune dysregulation, polyendocrinopathy, enteropathy, X-linked) syndrome, a potentially lethal disease characterized by autoimmune/allergic multiorgan damage due to the lack of regulatory T cells.
  • Certain Oncology therapies inhibit immune tolerance to promote elimination of neoplastic cells. For example, the monoclonal antibodies ipilimumab (anti-CTLA-4), nivolumab (anti-PD-1) and atezolizumab (anti-PD-L1).

2. Develop and share own educational resources.

For example, when learning about interleukin-4 (IL-4), a key cytokine involved in the pathogenesis of TH2-mediated allergic diseases:

  • IL-4 is a cytokine that induces TH2 immunity through 2 receptors: a) type 1 receptor, formed by IL-4Rα chain and the common gamma chain; b) type 2 receptor, formed by IL-4Rα chain and IL-13Rα chain (IL-13 also signals through this type 2 receptor).

  • The main sources of IL-4 are TH2 lymphocytes, type 2 innate lymphoid cells (ILC2), basophils, mast cells and eosinophils. Physiologically, IL-4 strengthens our TH2 army against helminths and other extracellular parasites by inducing development of TH2 cells and secretion of IgE from B lymphocytes.

  • Excessive production of IL-4 against molecules that should be tolerated favors the development of TH2 allergic diseases, such as allergic bronchial asthma, allergic rhinitis and atopic dermatitis. In patients with these diseases, IL-4 and its receptor are therapeutic targets for novel drugs. For example: a) Pitrakinra is a mutated recombinant version of IL-4 that binds to the IL-4Rα subunit, thereby blocking the action of interleukins 4 and 13; b) Pascolizumab is a humanized anti-IL-4 monoclonal antibody investigated as an asthma therapy; c) The monoclonal antibody Dupilumab is directed against the IL-4Rα subunit of the IL-4 receptor. It blocks the activity of IL-4 and IL-13, becoming one of the most promising drugs for the treatment of TH2 allergies.

References:

  • Attias M, Al-Aubodah T, Piccirillo CA. Mechanisms of human FoxP3+ Treg cell development and function in health and disease. Clin Exp Immunol. 2019; 197(1): 36-51.
  • Wang H, Kaur G, Sankin AI, Chen F, Guan F, Zang X. Immune checkpoint blockade and CAR-T cell therapy in hematologic malignancies. J Hematol Oncol. 2019;12(1): 59.
  • Akdis M, Aab A, Altunbulakli C, Azkur K, Costa RA, Crameri R, et al. Interleukins (from IL-1 to IL-38), interferons, transforming growth factor β, and TNF-α: Receptors, functions, and roles in diseases. J Allergy Clin Immunol. 2016;138(4): 984-1010.
  • Aldave JC. The interleukins. Self-educational resources.