Allergic conjunctivitis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sujaya Chattopadhyay, M.D.[2]
Overview
The ocular allergic response is a cascade of events that is coordinated by mast cells.[1]
Pathophysiology
Allergic conjunctivitis is the manifestation of a predominantly IgE-mediated hypersensitivity reaction[2].
Stimulated mast cells release increased amounts of tryptase, histamine, prostaglandins and leukotrienes in tears. This is the immediate response, which lasts for the initial 20-30 min.
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Degranulation of mast cells activates vascular endothelial cells to express adhesion molecules such as intercellular adhesion molecule (ICAM), vascular cell adhesion molecule (VCAM) and release chemokines like regulated upon activation normal T cells expressed and secreted (RANTES), monocyte chemoattractant protein (MCP), Interleukin (IL)-8, eotaxin, macrophage inflammatory protein (MIP)-1 alpha.
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Triggers the recruitment of inflammatory cells in the conjunctival mucosa, which mediate the ocular late-phase reaction[3].
Pathophysiologic characteristics of special forms of allergic conjunctivitis
- The allergic reaction in VKC is chronic in nature, mediated by Th2-lymphocyte alongside the over-expression of mast cells, eosinophils, neutrophils, Th2-derived cytokines, chemokines, adhesion molecules, growth factors, fibroblasts and lymphocytes. IL-4 and IL-13 are involved in the formation of the giant papillae by inducing extra-cellular matrix production and conjunctival fibroblast proliferation[4].
- Th1 lymphocytes are one of the primary mediators in AKC[5].
- Contact allergy, or allergic contact dermatitis, in contrast is a type-IV delayed hypersensitivity response[6]
Antigen-MHC class II complex interacts with T-lymphocytes → Differentiation of CD4+ T-lymphocyte into memory T-lymphocyte→ Proliferates to release cytokines[7]. Th1 derived cytokines, such as IL-2, IL-3, IFN-γ, recruit macrophages. Th2 derived cytokines, such as IL-4 and IL-5, mediate the activation and chemotaxis of eosinophils[8].
- IL-17-producing T cells (Th-17 cells) and regulatory T cells (Treg cells) have also been found to be contributing to the pathogenesis. However, their role has not yet been clearly elucidated[9].
References
- ↑ Liu G, Keane-Myers A, Miyazaki D, Tai A, Ono SJ (1999). "Molecular and cellular aspects of allergic conjunctivitis". Chem. Immunol. Chemical Immunology and Allergy. 73: 39–58. doi:10.1159/000058748. ISBN 3-8055-6893-2. PMID 10590573.
- ↑ La Rosa M, Lionetti E, Reibaldi M, Russo A, Longo A, Leonardi S; et al. (2013). "Allergic conjunctivitis: a comprehensive review of the literature". Ital J Pediatr. 39: 18. doi:10.1186/1824-7288-39-18. PMC 3640929. PMID 23497516.
- ↑ Leonardi A (2002). "The central role of conjunctival mast cells in the pathogenesis of ocular allergy". Curr Allergy Asthma Rep. 2 (4): 325–31. doi:10.1007/s11882-002-0061-7. PMID 12044269.
- ↑ Leonardi A, Secchi AG (2003). "Vernal keratoconjunctivitis". Int Ophthalmol Clin. 43 (1): 41–58. doi:10.1097/00004397-200343010-00007. PMID 12544394.
- ↑ Bonini S (2004). "Atopic keratoconjunctivitis". Allergy. 59 Suppl 78: 71–3. doi:10.1111/j.1398-9995.2004.00570.x. PMID 15245362.
- ↑ Niederkorn JY (2008). "Immune regulatory mechanisms in allergic conjunctivitis: insights from mouse models". Curr Opin Allergy Clin Immunol. 8 (5): 472–6. doi:10.1097/ACI.0b013e32830edbcb. PMC 2559965. PMID 18769204.
- ↑ Niederkorn JY, Chen PW, Mellon J, Stevens C, Mayhew E (2010). "Allergic conjunctivitis exacerbates corneal allograft rejection by activating Th1 and th2 alloimmune responses". J Immunol. 184 (11): 6076–83. doi:10.4049/jimmunol.0902300. PMC 2910911. PMID 20410484.
- ↑ Mosmann TR, Coffman RL (1989). "TH1 and TH2 cells: different patterns of lymphokine secretion lead to different functional properties". Annu Rev Immunol. 7: 145–73. doi:10.1146/annurev.iy.07.040189.001045. PMID 2523712.
- ↑ Oboki K, Ohno T, Saito H, Nakae S (2008). "Th17 and allergy". Allergol Int. 57 (2): 121–34. doi:10.2332/allergolint.R-07-160. PMID 18427165.