IL-10 family
In addition to IL-10, it includes IL-19, IL-20, IL-22, IL-24 and IL-26.[1]
The IL10 family is a family of interleukins.
Some sources also include the interferons IL-28 and IL-29.[2]
IL-10 Family
Biological activity
IL-10 family - is one of the important types of cytokines, that can stop the inflammation. In general. these cytokines have a helical structure of homodimers.[3] The difference that the members of IL-10 family have between each other is that they have various receptor-binding residues, which help with interaction with specific cytokine receptors.[4]
IL-10
Interleukin 10 is produced by regulatory T lymphocytes, B cells, and monocytes. It is a homodimer that functions through the IL-10R1 and IL-10R2 receptor complexes, activating such kinases as Janus kinase and tyrosine kinase 2.[5] IL-10R2 receptor is presented in most cells, when IL-10R1 receptor is IL-10 is also an inhibitor of expressions of CD80 and CD86 by dendritic cells (DC) and antigen-presenting cells (APC),[5] and of T cells, decreasing their cytokine production, therefore, controlling their activation. IL-10 plays a big role in regulating allergies by inhibiting cytokines responsible for allergic inflammation.
IL-19
Interleukin 19 is produced mainly in monocytes, and can be found in big concentrations in patients with allergic disorders and psoriasis. IL-19 plays a big role in the CNS by regulating the inflammation process through a delayed production of it.[6]
IL-20
IL-20 - induces cheratin proliferation and Stat-3 signal transduction pathway;[6] is expressed in the CNS, myeloid cells, and keratinocytes. When IL-20 is inhibited in the CNS can stop such inflammations as acute ischemic brain injury.[6][5]
IL-22
IL-22 mediates inflammation and binds class II cytokine receptor heterodimers IL-22 RA1/CRF2-4;[7] is involved in immuno-regulatory responses
IL-24
IL-24 produced by activated monocytes and T-cells.[8]
IL-26
IL-26 is a newly discovered cytokine produced by memory T cells and monocytes. IL-26 assist with the process of human T cell transformation after their infections.[8]
References
- Conti P, Kempuraj D, Frydas S, et al. (September 2003). "IL-10 subfamily members: IL-19, IL-20, IL-22, IL-24 and IL-26". Immunol. Lett. 88 (3): 171–4. doi:10.1016/S0165-2478(03)00087-7. PMID 12941475.
- Commins S, Steinke JW, Borish L (May 2008). "The extended IL-10 superfamily: IL-10, IL-19, IL-20, IL-22, IL-24, IL-26, IL-28, and IL-29". J. Allergy Clin. Immunol. 121 (5): 1108–11. doi:10.1016/j.jaci.2008.02.026. PMID 18405958.
- Fickenscher, Helmut; Hör, Simon; Küpers, Heide; Knappe, Andrea; Wittmann, Sabine; Sticht, Heinrich (2002-02-01). "The interleukin-10 family of cytokines". Trends in Immunology. 23 (2): 89–96. doi:10.1016/S1471-4906(01)02149-4. ISSN 1471-4906.
- Trivella, Daniela Barretto Barbosa; Ferreira-Júnior, José Ribamar; Dumoutier, Laure; Renauld, Jean-Christophe; Polikarpov, Igor (September 2010). "Structure and function of interleukin-22 and other members of the interleukin-10 family". Cellular and Molecular Life Sciences. 67 (17): 2909–2935. doi:10.1007/s00018-010-0380-0. ISSN 1420-682X.
- Commins, Scott; Steinke, John W.; Borish, Larry (2008-05-01). "The extended IL-10 superfamily: IL-10, IL-19, IL-20, IL-22, IL-24, IL-26, IL-28, and IL-29". Journal of Allergy and Clinical Immunology. 121 (5): 1108–1111. doi:10.1016/j.jaci.2008.02.026. ISSN 0091-6749. PMID 18405958.
- Burmeister, Amanda R.; Marriott, Ian (2018). "The Interleukin-10 Family of Cytokines and Their Role in the CNS". Frontiers in Cellular Neuroscience. 12. doi:10.3389/fncel.2018.00458. ISSN 1662-5102.
- Lerner, Ulf H. (2020-01-01), Zaidi, Mone (ed.), "Role of Interleukins on Physiological and Pathological Bone Resorption and Bone Formation: Effects by Cytokines in The IL-6 and IL-10 Families", Encyclopedia of Bone Biology, Oxford: Academic Press, pp. 67–87, ISBN 978-0-12-814082-6, retrieved 2020-11-24
- Scrivo, R.; Conigliaro, P.; Riccieri, V.; Di Franco, M.; Alessandri, C.; Spadaro, A.; Perricone, R.; Valesini, G. "Distribution of interleukin-10 family cytokines in serum and synovial fluid of patients with inflammatory arthritis reveals different contribution to systemic and joint inflammation".