Sandbox:Shalinder: Difference between revisions
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**Filaggrin is one of the major determinants of barrier function.<ref name="pmid21991953">{{cite journal |vauthors=Irvine AD, McLean WH, Leung DY |title=Filaggrin mutations associated with skin and allergic diseases |journal=N. Engl. J. Med. |volume=365 |issue=14 |pages=1315–27 |date=October 2011 |pmid=21991953 |doi=10.1056/NEJMra1011040 |url=}}</ref>. Encoded by the FLG gene, filaggrin monomers constitute keratin-filament-aggregating properties. | **Filaggrin is one of the major determinants of barrier function.<ref name="pmid21991953">{{cite journal |vauthors=Irvine AD, McLean WH, Leung DY |title=Filaggrin mutations associated with skin and allergic diseases |journal=N. Engl. J. Med. |volume=365 |issue=14 |pages=1315–27 |date=October 2011 |pmid=21991953 |doi=10.1056/NEJMra1011040 |url=}}</ref>. Encoded by the FLG gene, filaggrin monomers constitute keratin-filament-aggregating properties. | ||
**Following its synthesis primarily as profilaggrin, it undergoes extensive phosphorylation, resulting in the formation of filaggrin monomers, which on further breakdown are major components of the natural moisturizer factor (NMF).<ref name="pmid19386895">{{cite journal |vauthors=Sandilands A, Sutherland C, Irvine AD, McLean WH |title=Filaggrin in the frontline: role in skin barrier function and disease |journal=J. Cell. Sci. |volume=122 |issue=Pt 9 |pages=1285–94 |date=May 2009 |pmid=19386895 |pmc=2721001 |doi=10.1242/jcs.033969 |url=}}</ref> | **Following its synthesis primarily as profilaggrin, it undergoes extensive phosphorylation, resulting in the formation of filaggrin monomers, which on further breakdown are major components of the natural moisturizer factor (NMF).<ref name="pmid19386895">{{cite journal |vauthors=Sandilands A, Sutherland C, Irvine AD, McLean WH |title=Filaggrin in the frontline: role in skin barrier function and disease |journal=J. Cell. Sci. |volume=122 |issue=Pt 9 |pages=1285–94 |date=May 2009 |pmid=19386895 |pmc=2721001 |doi=10.1242/jcs.033969 |url=}}</ref> | ||
**The main function of natural moisturizer factor is to maintains skin hydration and water retention within the stratum corneum. | |||
===Pathogenesis=== | ===Pathogenesis=== | ||
Revision as of 16:16, 27 September 2018
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Shalinder Singh, M.B.B.S.[2]
Overview
It is thought that Atopic dermatitis is caused by either skin barrier dysfunction or immune dysregulation.
Pathophysiology
Physiology
The normal physiology of skin barrier function and immune regulation can be understood as follows:
- Skin Barrier: In the epidermis, stratum corneum consisting of stacks of anucleate corneocytes filled with keratin filaments serves as the first line of defense between the body and the environment.[1] Interactions between terminally differentiated keratinocytes and structural proteins such as lipids, regulatory enzymes, and filaggrin, determine the permeability of epidermis.
- Filaggrin is one of the major determinants of barrier function.[2]. Encoded by the FLG gene, filaggrin monomers constitute keratin-filament-aggregating properties.
- Following its synthesis primarily as profilaggrin, it undergoes extensive phosphorylation, resulting in the formation of filaggrin monomers, which on further breakdown are major components of the natural moisturizer factor (NMF).[3]
- The main function of natural moisturizer factor is to maintains skin hydration and water retention within the stratum corneum.
Pathogenesis
- The exact pathogenesis of [disease name] is not completely understood.
OR
- It is understood that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
Genetics
[Disease name] is transmitted in [mode of genetic transmission] pattern.
OR
Genes involved in the pathogenesis of [disease name] include:
- [Gene1]
- [Gene2]
- [Gene3]
OR
The development of [disease name] is the result of multiple genetic mutations such as:
- [Mutation 1]
- [Mutation 2]
- [Mutation 3]
Associated Conditions
Conditions associated with [disease name] include:
- [Condition 1]
- [Condition 2]
- [Condition 3]
Gross Pathology
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ Elias PM, Wakefield JS (October 2014). "Mechanisms of abnormal lamellar body secretion and the dysfunctional skin barrier in patients with atopic dermatitis". J. Allergy Clin. Immunol. 134 (4): 781–791.e1. doi:10.1016/j.jaci.2014.05.048. PMC 4186911. PMID 25131691.
- ↑ Irvine AD, McLean WH, Leung DY (October 2011). "Filaggrin mutations associated with skin and allergic diseases". N. Engl. J. Med. 365 (14): 1315–27. doi:10.1056/NEJMra1011040. PMID 21991953.
- ↑ Sandilands A, Sutherland C, Irvine AD, McLean WH (May 2009). "Filaggrin in the frontline: role in skin barrier function and disease". J. Cell. Sci. 122 (Pt 9): 1285–94. doi:10.1242/jcs.033969. PMC 2721001. PMID 19386895.