Psoriasis causes: Difference between revisions
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===Common Causes=== | ===Common Causes=== | ||
==== Genetics ==== | ==== Genetics<ref name="pmid16916825">{{cite journal |vauthors=Smith CH, Barker JN |title=Psoriasis and its management |journal=BMJ |volume=333 |issue=7564 |pages=380–4 |year=2006 |pmid=16916825 |pmc=1550454 |doi=10.1136/bmj.333.7564.380 |url=}}</ref> ==== | ||
* The human genome has at least nine different loci , which lead to the development of psoriasis (PSORS1-9). | * The human genome has at least nine different loci , which lead to the development of psoriasis (PSORS1-9). | ||
* PSORS-1, a part of the major histocompatibility complex (MHC) on chromosome 6p2, is the major genetic determinant of psoriasis, and is responsible for up to fifty percent of genetic susceptibility to the disease.<ref name="pmid16138103">{{cite journal |vauthors=Bowcock AM, Krueger JG |title=Getting under the skin: the immunogenetics of psoriasis |journal=Nat. Rev. Immunol. |volume=5 |issue=9 |pages=699–711 |year=2005 |pmid=16138103 |doi=10.1038/nri1689 |url=}}</ref> | * PSORS-1, a part of the major histocompatibility complex (MHC) on chromosome 6p2, is the major genetic determinant of psoriasis, and is responsible for up to fifty percent of genetic susceptibility to the disease.<ref name="pmid16138103">{{cite journal |vauthors=Bowcock AM, Krueger JG |title=Getting under the skin: the immunogenetics of psoriasis |journal=Nat. Rev. Immunol. |volume=5 |issue=9 |pages=699–711 |year=2005 |pmid=16138103 |doi=10.1038/nri1689 |url=}}</ref> | ||
* Misssense mutations in CARD14 gene lead to activation of the NF-κB pathway | * The second most well-characterized disease-susceptibility locus (''PSORS2'') is found within 17q24–q25. | ||
* Misssense mutations in CARD14 gene lead to activation of the NF-κB pathway. | |||
* Another major gene involved in the development of psoriasis is a HLA class I allele, specifically HLA-Cw6.<ref name="pmid7387872">{{cite journal |vauthors=Tiilikainen A, Lassus A, Karvonen J, Vartiainen P, Julin M |title=Psoriasis and HLA-Cw6 |journal=Br. J. Dermatol. |volume=102 |issue=2 |pages=179–84 |year=1980 |pmid=7387872 |doi= |url=}}</ref> | |||
==== Immune system ==== | ==== Immune system ==== | ||
* Both innate and adaptive immunity is involved in the development of psoriasis. | * Both innate and adaptive immunity is involved in the development of psoriasis. | ||
* The key cytokines of immune system, which lead to psoriasis are tumor necrosis factor-alpha and interferon alpha. | * The key cytokines of immune system, which lead to psoriasis are tumor necrosis factor-alpha and interferon alpha. | ||
* The LFA-1 integrin is also important in the immune pathogenesis of psoriasis and has been known to be a target for medications used for the management of psoriasis. | |||
* Within the immune system, development of psoriasis is based upon four key pathways/interactions: | * Within the immune system, development of psoriasis is based upon four key pathways/interactions: | ||
** Antigen presentation | ** Antigen presentation | ||
| Line 26: | Line 29: | ||
==== Environmental and behavioral ==== | ==== Environmental and behavioral ==== | ||
The enviromental factors implicated in the development or aggravation of psoriasis are:<ref>[http://www.skincarephysicians.com/psoriasisnet/triggers.html <nowiki>[1]</nowiki>] Psoriasis Triggers at Psoriasis Net. SkinCarePhysicians.com 9-28-05. American Academy of Dermatology, 2008.</ref><ref>{{cite journal |author=Behnam SM, Behnam SE, Koo JY |title=Smoking and psoriasis |journal=Skinmed |volume=4 |issue=3 |pages=174–6 |year=2005 |pmid=15891254 |doi= |url=http://www.lejacq.com/articleDetail.cfm?pid=SKINmed_4;3:174}}</ref><ref>[http://www.medscape.com/viewarticle/556533 <nowiki>[2]</nowiki>][http://dermatology.cdlib.org/132/reviews/HIV/fife.html <nowiki>[3]</nowiki>] Fife, Jeffes, Koo, Waller. Unraveling the Paradoxes of HIV-associated Psoriasis: A Review of T-cell Subsets and Cytokine Profiles. 5-18-07. Retrieved 5-13-08.</ref><ref>{{cite journal |author=Ortonne JP, Lebwohl M, Em Griffiths C |title=Alefacept-induced decreases in circulating blood lymphocyte counts correlate with clinical response in patients with chronic plaque psoriasis |journal=Eur J Dermatol |volume=13 |issue=2 |pages=117–23 |year=2003 |pmid=12695125 |doi= |url=http://www.john-libbey-eurotext.fr/medline.md?issn=1167-1122&vol=13&iss=2&page=117}}</ref><ref>{{cite journal |author=Austin LM, Ozawa M, Kikuchi T, Walters IB, Krueger JG |title=The majority of epidermal T cells in Psoriasis vulgaris lesions can produce type 1 cytokines, interferon-gamma, interleukin-2, and tumor necrosis factor-alpha, defining TC1 (cytotoxic T lymphocyte) and TH1 effector populations: a type 1 differentiation bias is also measured in circulating blood T cells in psoriatic patients |journal=J. Invest. Dermatol. |volume=113 |issue=5 |pages=752–9 |year=1999 |month=November |pmid=10571730 |doi=10.1046/j.1523-1747.1999.00749.x |url=}}</ref><ref>[http://www.nsc.gov.sg/cgi-bin/WB_ContentGen.pl?id=401&gid=83 <nowiki>[4]</nowiki>] A Case Report of Severe Psoriasis in a Patient with AIDS: The Role of the HIV Virus and the Therapeutic Challenges Involved. Vol: 13 No 2, 2002. National Skin Center. Retrieved 05-13-08.</ref> | The enviromental factors implicated in the development or aggravation of psoriasis are:<ref>[http://www.skincarephysicians.com/psoriasisnet/triggers.html <nowiki>[1]</nowiki>] Psoriasis Triggers at Psoriasis Net. SkinCarePhysicians.com 9-28-05. American Academy of Dermatology, 2008.</ref><ref>{{cite journal |author=Behnam SM, Behnam SE, Koo JY |title=Smoking and psoriasis |journal=Skinmed |volume=4 |issue=3 |pages=174–6 |year=2005 |pmid=15891254 |doi= |url=http://www.lejacq.com/articleDetail.cfm?pid=SKINmed_4;3:174}}</ref><ref>[http://www.medscape.com/viewarticle/556533 <nowiki>[2]</nowiki>][http://dermatology.cdlib.org/132/reviews/HIV/fife.html <nowiki>[3]</nowiki>] Fife, Jeffes, Koo, Waller. Unraveling the Paradoxes of HIV-associated Psoriasis: A Review of T-cell Subsets and Cytokine Profiles. 5-18-07. Retrieved 5-13-08.</ref><ref>{{cite journal |author=Ortonne JP, Lebwohl M, Em Griffiths C |title=Alefacept-induced decreases in circulating blood lymphocyte counts correlate with clinical response in patients with chronic plaque psoriasis |journal=Eur J Dermatol |volume=13 |issue=2 |pages=117–23 |year=2003 |pmid=12695125 |doi= |url=http://www.john-libbey-eurotext.fr/medline.md?issn=1167-1122&vol=13&iss=2&page=117}}</ref><ref>{{cite journal |author=Austin LM, Ozawa M, Kikuchi T, Walters IB, Krueger JG |title=The majority of epidermal T cells in Psoriasis vulgaris lesions can produce type 1 cytokines, interferon-gamma, interleukin-2, and tumor necrosis factor-alpha, defining TC1 (cytotoxic T lymphocyte) and TH1 effector populations: a type 1 differentiation bias is also measured in circulating blood T cells in psoriatic patients |journal=J. Invest. Dermatol. |volume=113 |issue=5 |pages=752–9 |year=1999 |month=November |pmid=10571730 |doi=10.1046/j.1523-1747.1999.00749.x |url=}}</ref><ref>[http://www.nsc.gov.sg/cgi-bin/WB_ContentGen.pl?id=401&gid=83 <nowiki>[4]</nowiki>] A Case Report of Severe Psoriasis in a Patient with AIDS: The Role of the HIV Virus and the Therapeutic Challenges Involved. Vol: 13 No 2, 2002. National Skin Center. Retrieved 05-13-08.</ref><ref name="pmid15199399">{{cite journal |vauthors=Nickoloff BJ, Nestle FO |title=Recent insights into the immunopathogenesis of psoriasis provide new therapeutic opportunities |journal=J. Clin. Invest. |volume=113 |issue=12 |pages=1664–75 |year=2004 |pmid=15199399 |pmc=420513 |doi=10.1172/JCI22147 |url=}}</ref> | ||
** Stress (physical and mental) | ** Stress (physical and mental) | ||
** Smoking | ** Smoking | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Psoriasis is caused due to complex interactions between the genetics, immune system and environmental factors.
Causes
Common Causes
Genetics[1]
- The human genome has at least nine different loci , which lead to the development of psoriasis (PSORS1-9).
- PSORS-1, a part of the major histocompatibility complex (MHC) on chromosome 6p2, is the major genetic determinant of psoriasis, and is responsible for up to fifty percent of genetic susceptibility to the disease.[2]
- The second most well-characterized disease-susceptibility locus (PSORS2) is found within 17q24–q25.
- Misssense mutations in CARD14 gene lead to activation of the NF-κB pathway.
- Another major gene involved in the development of psoriasis is a HLA class I allele, specifically HLA-Cw6.[3]
Immune system
- Both innate and adaptive immunity is involved in the development of psoriasis.
- The key cytokines of immune system, which lead to psoriasis are tumor necrosis factor-alpha and interferon alpha.
- The LFA-1 integrin is also important in the immune pathogenesis of psoriasis and has been known to be a target for medications used for the management of psoriasis.
- Within the immune system, development of psoriasis is based upon four key pathways/interactions:
- Antigen presentation
- NF-κB signaling
- IL-23/IL-17 axis
- Type I IFN pathway.
Environmental and behavioral
The enviromental factors implicated in the development or aggravation of psoriasis are:[4][5][6][7][8][9][10]
- Stress (physical and mental)
- Smoking
- Excessive alcohol consumption
- Infection (Streptococcal, HIV
- Seasonal variation
- Medications (Lithium, Beta blockers, pegylated interferon alpha-2b, Siltuximab)
- Obesity
- Skin injury
- Skin dryness
References
- ↑ Smith CH, Barker JN (2006). "Psoriasis and its management". BMJ. 333 (7564): 380–4. doi:10.1136/bmj.333.7564.380. PMC 1550454. PMID 16916825.
- ↑ Bowcock AM, Krueger JG (2005). "Getting under the skin: the immunogenetics of psoriasis". Nat. Rev. Immunol. 5 (9): 699–711. doi:10.1038/nri1689. PMID 16138103.
- ↑ Tiilikainen A, Lassus A, Karvonen J, Vartiainen P, Julin M (1980). "Psoriasis and HLA-Cw6". Br. J. Dermatol. 102 (2): 179–84. PMID 7387872.
- ↑ [1] Psoriasis Triggers at Psoriasis Net. SkinCarePhysicians.com 9-28-05. American Academy of Dermatology, 2008.
- ↑ Behnam SM, Behnam SE, Koo JY (2005). "Smoking and psoriasis". Skinmed. 4 (3): 174–6. PMID 15891254.
- ↑ [2][3] Fife, Jeffes, Koo, Waller. Unraveling the Paradoxes of HIV-associated Psoriasis: A Review of T-cell Subsets and Cytokine Profiles. 5-18-07. Retrieved 5-13-08.
- ↑ Ortonne JP, Lebwohl M, Em Griffiths C (2003). "Alefacept-induced decreases in circulating blood lymphocyte counts correlate with clinical response in patients with chronic plaque psoriasis". Eur J Dermatol. 13 (2): 117–23. PMID 12695125.
- ↑ Austin LM, Ozawa M, Kikuchi T, Walters IB, Krueger JG (1999). "The majority of epidermal T cells in Psoriasis vulgaris lesions can produce type 1 cytokines, interferon-gamma, interleukin-2, and tumor necrosis factor-alpha, defining TC1 (cytotoxic T lymphocyte) and TH1 effector populations: a type 1 differentiation bias is also measured in circulating blood T cells in psoriatic patients". J. Invest. Dermatol. 113 (5): 752–9. doi:10.1046/j.1523-1747.1999.00749.x. PMID 10571730. Unknown parameter
|month=ignored (help) - ↑ [4] A Case Report of Severe Psoriasis in a Patient with AIDS: The Role of the HIV Virus and the Therapeutic Challenges Involved. Vol: 13 No 2, 2002. National Skin Center. Retrieved 05-13-08.
- ↑ Nickoloff BJ, Nestle FO (2004). "Recent insights into the immunopathogenesis of psoriasis provide new therapeutic opportunities". J. Clin. Invest. 113 (12): 1664–75. doi:10.1172/JCI22147. PMC 420513. PMID 15199399.