Is Human Papillomavirus Type 5 the Putative Autoantigen Involved in Psoriasis?

Majewski, Slavomir; Jabłońska, Stefania; Favre, Michel; Orth, Gérard

doi:10.1046/j.1523-1747.1998.00310.x

Cited by 28 publications

(31 citation statements)

References 19 publications

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“…U chorych w około 90% wykwitów wykryto DNA HPV5 i inne związane z nim genotypy EV-HPV. Dodatkowo locus podatności na zakażenia HPV-EV znajduje się na chromosomie 17q w regionie PSORS 2 [58][59][60]. Badacze sugerują, że na początku w łuszczycy istnieje zjawisko poliklonalnej aktywacji komórek T, najprawdopodobniej wywołanej przez superantygeny lub uraz naskórka (objaw Köbnera), natomiast w późniejszej fazie autoreaktywne limfocyty T rozpoznają autoantygeny (białka kapsydu L1 HPV5) w naskórku, co prowadzi do reakcji autoimmunologicznej [61].…”

Section: Autoantygeny W łUszczycyunclassified

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Psoriasis as an autoimmune disease

Owczarczyk‐Saczonek¹,

Placek²

2014

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StreSzczenieObecnie uważa się, że łuszczyca należy do kręgu schorzeń autoimmunologicznych, współistniejących z innymi chorobami z tej grupy. U pacjentów stwierdza się najczęściej łuszczycowe zapalenie stawów, reumatoidalne zapalenie stawów, choroby tkanki łącznej, stwardnienie rozsiane, autoimmunologiczne choroby tarczycy, celiakię, nieswoiste zapalenia jelit. Współwystępowanie tych zaburzeń może stanowić problem diagnostyczny i leczniczy (kontrowersje dotyczące stosowania kortykosteroidów). Wspólna patogeneza pozostaje nadal nie do końca wyjaśniona. Uważa się, że utrata immunotolerancji prowadzi do powstania m.in. autoreaktywnych limfocytów Th1 i Th17, które rozpoznają autoantygeny i prowadzą do ich niszczenia w danym narządzie docelowym. Pewne cechy mechanizmów immunologicznych obserwowanych w łuszczycy sugerują jej autoimmunologiczne tło. Należą do nich uwarunkowania genetyczne, np. PSORS 3 na chromosomie 4q predysponuje do celiakii, cukrzycy typu 1, choroby Gravesa-Basedowa i reumatoidalnego zapalenia stawów. Łuszczyca jest chorobą, w któ-rej decydującą rolę odgrywa aktywacja osi IL-12/Th1/IFN-γ i Th17/ IL-23. Prawdopodobnie IL-12 działa na naiwne limfocyty T i zapocząt-kowuje odpowiedź Th1, a IL-23 podtrzymuje reakcję zapalną mediowaną przez Th1, pobudza dojrzewanie i aktywność Th17 oraz wpływa na utrzymanie odpowiedniej puli komórek pamięci. Dochodzi również do zaburzenia funkcji limfocytów Treg, odpowiedzialnych za niszczenie limfocytów autoreaktywnych. Ponadto keratynocyty łuszczycowe mają zwiększoną oporność na apoptozę, której zadaniem jest eliminacja uszkodzonych komórek, aby nie zostały rozpoznane jako antygenowo obce. Badacze sugerują jednak, że początkowo następuje poliklonalna aktywacja limfocytów T wywołana przez superantygeny (m.in. paciorkowcowe białka M, peptydoglikan) lub uraz naskórka (objaw Köbne-ra), natomiast w późniejszej fazie autoreaktywne limfocyty T rozpoznają autoantygeny (keratyna 17, białka kapsydu L1 HPV 5, Pso p27) w naskórku, co prowadzi do reakcji autoimmunologicznej. AbStrActNowadays it is known that psoriasis belongs to the group of autoimmune diseases and may coexist with other diseases in this group. Most often patients have psoriatic arthritis, rheumatoid arthritis, inflammatory bowel disease, autoimmune thyroid diseases and multiple sclerosis. The coexistence of these disorders can be a diagnostic and therapeutic problem (there is controversy over the use of corticosteroids). The common pathogenesis is still not explained. We know that the loss of immunotolerance leads to formation of autoreactive Th1 and Th17 lym-

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Section: Autoantygeny W łUszczycyunclassified

“…Może to wywołać aktywację dopełniacza, chemotaksję neutrofilów do warstwy rogowej i powstanie mikroropni Munro, co jest unikalną cechą łusz-czycy. Inne chemotaktyczne bodźce, takie jak IL-8 i produkty metabolizmu kwasu arachidonowego, mogą się przyczynić do dalszej rekrutacji leukocytów [58,59].…”

Section: Autoantygeny W łUszczycyunclassified

Psoriasis as an autoimmune disease

Owczarczyk‐Saczonek¹,

Placek²

2014

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“…On top of that, beta-HPV DNA has been detected in nearly all psoriasis patients tested, demonstrating that psoriatic individuals have an alleviated restriction toward HPV. As psoriasis is a common dermatosis affecting 2 to 5% of the human population, regardless of a contribution of beta-HPV to the pathogenesis of this disease (130), it can be assumed that psoriatic patients constitute a reservoir for HPV (53). In addition, beta-HPV DNA sequences and HPV5 antibodies were detected in patients with bullous disease and autoimmune connective tissue disorders with cutaneous involvement as well as in burned subjects (52).…”

Section: Commensalic or Symbiotic Nature Of Beta-hpv?mentioning

confidence: 99%

The EVER Proteins as a Natural Barrier against Papillomaviruses: a New Insight into the Pathogenesis of Human Papillomavirus Infections

Łazarczyk

Cassonnet

Pons

et al. 2009

Microbiol Mol Biol Rev

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133

128

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SUMMARY Infections by human papillomaviruses (HPVs) are the most frequently occurring sexually transmitted diseases. The crucial role of genital oncogenic HPV in cervical carcinoma development is now well established. In contrast, the role of cutaneous HPV in skin cancer development remains a matter of debate. Cutaneous beta-HPV strains show an amazing ubiquity. The fact that a few oncogenic genotypes cause cancers in patients suffering from epidermodysplasia verruciformis is in sharp contrast to the unapparent course of infection in the general population. Our recent investigations revealed that a natural barrier exists in humans, which protects them against infection with these papillomaviruses. A central role in the function of this HPV-specific barrier is played by a complex of the zinc-transporting proteins EVER1, EVER2, and ZnT-1, which maintain cellular zinc homeostasis. Apparently, the deregulation of the cellular zinc balance emerges as an important step in the life cycles not only of cutaneous but also of genital HPVs, although the latter viruses have developed a mechanism by which they can break the barrier and impose a zinc imbalance. Herein, we present a previously unpublished list of the cellular partners of EVER proteins, which points to future directions concerning investigations of the mechanisms of action of the EVER/ZnT-1 complex. We also present a general overview of the pathogenesis of HPV infections, taking into account the latest discoveries regarding the role of cellular zinc homeostasis in the HPV life cycle. We propose a potential model for the mechanism of function of the anti-HPV barrier.

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“…Psoriasis is a T cell‐mediated inflammatory disease with the release of a number of cytokines that may lead to epidermal proliferation. The role of HPV5 in the pathogenesis of this disease is uncertain, and it has been postulated that the virus can act as a putative superantigen (3). On the contrary, other authors suggest that HPV infection does not play an active role in the pathogenesis of psoriasis but is latently present in the skin (4).…”

Section: Introductionmentioning

confidence: 99%

Human papillomavirus type 5 in primary keratinocytes from psoriatic skin

Simeone¹,

Teson

Latini

et al. 2005

Experimental Dermatology

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The role of human papillomaviruses (HPVs) in the pathogenesis of psoriasis is uncertain, and it has been postulated that the virus can act as a putative superantigen or it is activated from a latent status by inflammatory cytokines. To determine the involvement of HPV in the pathogenesis of psoriasis, primary cultures of keratinocytes from psoriatic lesions were analysed for the viral presence and for the production of inflammatory cytokines. Biopsies were taken from psoriatic lesions of 11 patients and from healthy donors undergoing plastic surgery. HPV DNA/RNAs were detected by nested polymerase chain reaction methods. The secretion of interleukin-6 (IL-6), IL-8 and IL-18 was determined in the conditioned medium by commercial enzyme-linked immunosorbent assay kits. Sixty-four per cent of the psoriatic keratinocytes were positive to HPV type 5 (HPV5), whereas no normal samples showed the presence of viral sequences. In the corresponding paraffin-embedded sections, multiple infection by HPV5 and HPV1 was detected. Comparable results in the production of inflammatory cytokines were obtained from HPV-infected vs. non-infected cell cultures. Specific HPV5 mRNAs were detected in the keratinocytes in the absence of cytokine stimulation, indicating that the expression of the viral genome may not be a consequence of the activation of the viral promoter by cytokines. The results are suggestive of an involvement of HPV5 in the psoriasis and reinforce the hypothesis that the replication of this virus in the psoriatic keratinocytes may cause the epidermal hyperproliferation as well as the antigen stimulation, which induces autoimmune phenomena.

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Is Human Papillomavirus Type 5 the Putative Autoantigen Involved in Psoriasis?

Cited by 28 publications

References 19 publications

Psoriasis as an autoimmune disease

Psoriasis as an autoimmune disease

The EVER Proteins as a Natural Barrier against Papillomaviruses: a New Insight into the Pathogenesis of Human Papillomavirus Infections

Human papillomavirus type 5 in primary keratinocytes from psoriatic skin

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