Allergic conjunctivitis pathophysiology: Difference between revisions
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{{Allergic conjunctivitis}} | {{Allergic conjunctivitis}} | ||
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== | ==Overview== | ||
[[Allergic]] [[conjunctivitis]] is a group of [[diseases]] affecting the [[ocular]] surface and is usually associated with type 1 [[hypersensitivity]] reactions. Two acute disorders, [[seasonal]] [[allergic]] [[conjunctivitis]] ([[SAC]]) and perennial [[allergic]] [[conjunctivitis]] ([[PAC]]) exist, as do three [[chronic]] [[diseases]], [[vernal]] [[keratoconjunctivitis]] ([[VKC]]), [[atopic]] [[keratoconjunctivitis]] ([[AKC]]), and giant [[papillary]] [[conjunctivitis]] ([[GPC]]). | |||
==[[Pathophysiology]]== | |||
[[Allergic]] [[conjunctivitis]] is the manifestation of a predominantly [[IgE]]-mediated [[hypersensitivity]] reaction<ref name="pmid23497516">{{cite journal| author=La Rosa M, Lionetti E, Reibaldi M, Russo A, Longo A, Leonardi S | display-authors=etal| title=Allergic conjunctivitis: a comprehensive review of the literature. | journal=Ital J Pediatr | year= 2013 | volume= 39 | issue= | pages= 18 | pmid=23497516 | doi=10.1186/1824-7288-39-18 | pmc=3640929 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23497516 }} </ref>. | |||
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. | |||
↓ | |||
[[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. | |||
↓ | |||
Triggers the recruitment of [[inflammatory]] cells in the [[conjunctival]] [[mucosa]], which mediate the [[ocular]] late-phase reaction<ref name="pmid12044269">{{cite journal| author=Leonardi A| title=The central role of conjunctival mast cells in the pathogenesis of ocular allergy. | journal=Curr Allergy Asthma Rep | year= 2002 | volume= 2 | issue= 4 | pages= 325-31 | pmid=12044269 | doi=10.1007/s11882-002-0061-7 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12044269 }} </ref>. | |||
===[[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<ref name="pmid12544394">{{cite journal| author=Leonardi A, Secchi AG| title=Vernal keratoconjunctivitis. | journal=Int Ophthalmol Clin | year= 2003 | volume= 43 | issue= 1 | pages= 41-58 | pmid=12544394 | doi=10.1097/00004397-200343010-00007 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12544394 }} </ref>. | |||
* [[Th1]] [[lymphocytes]] are one of the primary mediators in [[AKC]]<ref name="pmid15245362">{{cite journal| author=Bonini S| title=Atopic keratoconjunctivitis. | journal=Allergy | year= 2004 | volume= 59 Suppl 78 | issue= | pages= 71-3 | pmid=15245362 | doi=10.1111/j.1398-9995.2004.00570.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15245362 }} </ref>. | |||
* Contact [[allergy]], or [[allergic]] [[contact]] [[dermatitis]], in contrast is a type-IV delayed [[hypersensitivity]] response<ref name="pmid18769204">{{cite journal| author=Niederkorn JY| title=Immune regulatory mechanisms in allergic conjunctivitis: insights from mouse models. | journal=Curr Opin Allergy Clin Immunol | year= 2008 | volume= 8 | issue= 5 | pages= 472-6 | pmid=18769204 | doi=10.1097/ACI.0b013e32830edbcb | pmc=2559965 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18769204 }} </ref> | |||
[[Antigen-MHC]] class II complex interacts with [[T-lymphocytes]] → [[Differentiation]] of CD4+ [[T-lymphocyte]] into memory [[T-lymphocyte]]→ Proliferates to release [[cytokines]]<ref name="pmid20410484">{{cite journal| author=Niederkorn JY, Chen PW, Mellon J, Stevens C, Mayhew E| title=Allergic conjunctivitis exacerbates corneal allograft rejection by activating Th1 and th2 alloimmune responses. | journal=J Immunol | year= 2010 | volume= 184 | issue= 11 | pages= 6076-83 | pmid=20410484 | doi=10.4049/jimmunol.0902300 | pmc=2910911 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20410484 }} </ref>. [[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]]<ref name="pmid2523712">{{cite journal| author=Mosmann TR, Coffman RL| title=TH1 and TH2 cells: different patterns of lymphokine secretion lead to different functional properties. | journal=Annu Rev Immunol | year= 1989 | volume= 7 | issue= | pages= 145-73 | pmid=2523712 | doi=10.1146/annurev.iy.07.040189.001045 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2523712 }} </ref>. | |||
* [[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<ref name="pmid18427165">{{cite journal| author=Oboki K, Ohno T, Saito H, Nakae S| title=Th17 and allergy. | journal=Allergol Int | year= 2008 | volume= 57 | issue= 2 | pages= 121-34 | pmid=18427165 | doi=10.2332/allergolint.R-07-160 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18427165 }} </ref>. | |||
* In [[GPC]], the [[conjunctival]] [[tissues]] do not contain [[mast]] [[cells]], [[basophils]], or [[eosinophils]], to the extent of an [[allergic]] reaction. No increase in [[IgE]] or [[histaimine]] has been found in the [[tears]] of [[GPC]] patients. It appears that [[protein]] deposits on the surface of the contact lens become [[antigenic]] and stimulate the production of [[IgE]]; mechanical trauma and chronic irritation can also drive the release of some mediators ([[CXCL8]] and [[TNF-α]]) from the injured [[conjunctival]] [[epithelium]]<ref name="pmid18282547">{{cite journal| author=Donshik PC, Ehlers WH, Ballow M| title=Giant papillary conjunctivitis. | journal=Immunol Allergy Clin North Am | year= 2008 | volume= 28 | issue= 1 | pages= 83-103, vi | pmid=18282547 | doi=10.1016/j.iac.2007.11.001 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18282547 }} </ref>. | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
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{{WS}} | |||
[[Category:Disease]] | [[Category:Disease]] | ||
[[Category: | [[Category:Ophthalmology]] | ||
[[Category:Needs overview]] | |||
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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
Allergic conjunctivitis is a group of diseases affecting the ocular surface and is usually associated with type 1 hypersensitivity reactions. Two acute disorders, seasonal allergic conjunctivitis (SAC) and perennial allergic conjunctivitis (PAC) exist, as do three chronic diseases, vernal keratoconjunctivitis (VKC), atopic keratoconjunctivitis (AKC), and giant papillary conjunctivitis (GPC).
Pathophysiology
Allergic conjunctivitis is the manifestation of a predominantly IgE-mediated hypersensitivity reaction[1].
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.
↓
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.
↓
Triggers the recruitment of inflammatory cells in the conjunctival mucosa, which mediate the ocular late-phase reaction[2].
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[3].
- Th1 lymphocytes are one of the primary mediators in AKC[4].
- Contact allergy, or allergic contact dermatitis, in contrast is a type-IV delayed hypersensitivity response[5]
Antigen-MHC class II complex interacts with T-lymphocytes → Differentiation of CD4+ T-lymphocyte into memory T-lymphocyte→ Proliferates to release cytokines[6]. 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[7].
- 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[8].
- In GPC, the conjunctival tissues do not contain mast cells, basophils, or eosinophils, to the extent of an allergic reaction. No increase in IgE or histaimine has been found in the tears of GPC patients. It appears that protein deposits on the surface of the contact lens become antigenic and stimulate the production of IgE; mechanical trauma and chronic irritation can also drive the release of some mediators (CXCL8 and TNF-α) from the injured conjunctival epithelium[9].
References
- ↑ 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.
- ↑ Donshik PC, Ehlers WH, Ballow M (2008). "Giant papillary conjunctivitis". Immunol Allergy Clin North Am. 28 (1): 83–103, vi. doi:10.1016/j.iac.2007.11.001. PMID 18282547.