SavedAdd your journal

Journals / Fırat Tıp Dergisi / 2013 / Cilt: 18 - Sayı: 4

Immune response against to asthma

Astıma karşı oluşan immün yanıt

Gamze KIRKIL
Pages
191–197
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

But recently it is shown that Th1, Th9, Th17, Th25, folli- cular T cell, regulator T cell, invariant natural killer T cell, and γδ T cell contribute to the pathogenesis.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Both innate and adaptive immune responses develop against to asthma which is characterized by chronic inflammation of the airways.
📊
Key Findings & Data:It is known that contacting the products of microorganisms in early period of life changes the T helper (Th) 2 cell response to Th1 response.
💡
Conclusion & Impact:But recently it is shown that Th1, Th9, Th17, Th25, folli- cular T cell, regulator T cell, invariant natural killer T cell, and γδ T cell contribute to the pathogenesis.
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Both innate and adaptive immune responses develop against to asthma which is characterized by chronic inflammation of the airways. It is known that contacting the products of microorganisms in early period of life changes the T helper (Th) 2 cell response to Th1 response. Basic reseptors of innate immunity are toll-like receptors (TLR). Bronchial epitelial cells are the most important cells that take part in inflammation, these cells act as antigen presenting cells (APC), and they contribute to the airway remodelling by secreting some growth factors. The other cells in innate immunity are; dendritic cells, basophils, mast cells, eosinophils, monocytes, macrophages, platelets. Adaptive immune response occurs as cellular and humoral immunity. It is known for a long time that basic cells in asthma pathogenesis are Th2 cells. But recently it is shown that Th1, Th9, Th17, Th25, folli- cular T cell, regulator T cell, invariant natural killer T cell, and γδ T cell contribute to the pathogenesis.

Özet

Hava yollarının kronik inflamasyonu ile karakterize astıma karşı hem doğal hem de edinsel immün yanıt gelişmektedir. Hayatın erken döneminde mikrobik ürünler ile karşılaşmanın yardımcı T hücre (Th) 2 yanıtını Th1 yanıtına değiştirdiği bilinmektedir. Doğal immünitede temel rol oynayan reseptörler toll-like reseptörler (TLR)’dir. Bronş epitel hücreleri ise inflamasyonda rol alan en önemli hücrelerdir, bu hücreler antijen sunan hücre (APC) özelliği taşırlar, salgıladıkları birçok büyüme faktörü ile hava yolu yeniden yapılanmasına katkıda bulunurlar. Doğal immünitede rol alan diğer hücreler; dendritik hücreler, bazofiller, mast hücreleri, eozinofiller, monositler, makrofajlar, trombositlerdir. Edinsel immün yanıt ise hücresel ve hümöral immün yanıt şeklinde ortaya çıkmaktadır. Uzun süredir astım patogenezinde temel rol oynayan hücrelerin Th2 hücreler olduğu bilinmektedir. Ancak son zamanlarda Th1, Th9, Th17, Th25, folliküler T hücre, regülatör T hücre, invariant natural killer T hücreler ve γδ T hücrelerin de patogene- ze katkıda bulundukları gösterilmiştir.

🔖

Cite This Article

KIRKIL, G. (2013). Immune response against to asthma. Fırat Tıp Dergisi, Cilt: 18 - Sayı: 4, 191–197. https://ajindex.com/articles/214786

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (16)

  1. Beutler B. Innate immunity: an overview. Mol Immunol 2004; 40: 845-59
  2. Akira S, Takeda K. Toll-like receptor signalling. Nat Rev Immunol 2004; 4: 499-511
  3. Redecke V, Hacker H, Datta SK, et al. Cutting edge: activation of toll-like receptor 2 induces a Th2 immune response and promotes experimental asthma. J Immunol 2004; 172: 2739-43
  4. Velasco G, Campo M, Manrique OJ, et al. Toll-like receptor 4 or 2 agonists decrease allergic inflammation. Am J Respir Cell Mol Biol 2005; 32: 218-24
  5. Rosenstiel P, Jacobs G, Till A, Schreiber S. NOD-like recep- 6. Bach JF. The effect of infections on susceptibility to autoim- tors: ancient sentinels of the innate immune system. Cell Mol mune and allergic diseases. N Engl J Med 2002; 347: 911–20. Life Sci 2008; 65: 1361-77
  6. Bach JF. The effect of infections on susceptibility to autoim- mune and allergic diseases. N Engl J Med 2002; 347: 911–20
  7. Ouyang W, Kolls JK, Zheng Y. The biological functions of T helper 17 cell effector cytokines in inflammation. Immunity 2008; 28: 454-67
  8. Vignola AM, Campbell AM, Chanez P, Bousquet J, Michel FB, Godard P. HLA-DR and ICAM-1 expression on bronchial epit- helial cells in asthma and chronic bronchitis. Am Rev Respir Dis 1993; 148: 689-94
  9. Tanaka H, Maeda K, Nakamura Y, Azuma M, Yanagawa H, Sone S. CD40 and IFN-gamma dependent T cell activation by human bronchial epithelial cells. J Med Invest 2001; 48: 109- 17
  10. Wenzel SE. The significance of the neutrophil in asthma. Clin Exp Allergy Rev 2001; 1: 89-92
  11. Holgate S. Pathogenesis of asthma. In: Kay AB, Kaplan AF, Bousquet J, Holt PG (eds). Allergy and Allergic Disease. 2nd Ed. Blackwell Publishing 2008; 1608-31
  12. Yorgancıoğlu A. Astım patogenezi. In: Özlü T, Metintaş M, Karadağ M, Kaya A (eds). Solunum Hastalıkları. İstanbul Medikal Yayıncılık ve Ticaret AŞ 2010; 617-24
  13. Iwasaki A, Medzhitov R. Toll-like receptor control of the adaptive immune responses. Nat Immunol 2004; 5: 987-95
  14. Akbari O, Freeman GJ, Meyer EH, et al. Antigen-specific regulatory T cells develop via the ICOS-ICOS-ligand pathway and inhibit allergen-induced airway hyperreactivity. Nat Med 2002; 8: 1024-32
  15. Kaur D, Saunders R, Berger P, al. Airway smooth muscle and mast cell-derived CC chemokine ligand 19 mediate airway smooth muscle migration in asthma. Am J Respir Crit Care Med 2006; 174: 1179-88
  16. Barnes PJ, Djukanovic R, Holgate ST. Pathogenesis of asthma. Gibson GJ, Geddes GM, Costabel V, Sterk PJ, Corrin B (eds). Respi