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Study · Measured the body's own peptide · 2020

1 result

Paradoxical psoriasis induced by TNF-α blockade shows immunological features typical of the early phase of psoriasis development.

Fania L, Morelli M, Scarponi C, Mercurio L, Scopelliti F, Cattani C, Scaglione GL, Tonanzi T, Pilla MA, Pagnanelli G, Mazzanti C, Girolomoni G, Cavani A, Madonna S, Albanesi C

The journal of pathology. Clinical research29 Oct 2019Cited by 27 (Europe PMC)

PMID31577850 (opens in a new tab)PMCIDPMC6966707 (opens in a new tab)DOI10.1002/cjp2.147 (opens in a new tab)PepBankPUB-31577850
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Summary

Immunomodulation with anti-TNF-α is highly effective in the treatment of various immune-mediated inflammatory diseases, including hidradenitis suppurativa (HS). However, this may be responsible for unexpected paradoxical psoriasiform reactions. The pathogenic mechanisms underlying the induction of these events are not clear, even though the involvement of innate immune responses driven by plasmacytoid dendritic cells (pDC) has been described. In addition, the genetic predisposition to psoriasis of patients could be determinant. In this study, we investigated the immunological and genetic profiles of three HS patients without psoriasis who developed paradoxical psoriasiform reactions following anti-TNF-α therapy with adalimumab. We found that paradoxical psoriasiform skin reactions show immunological features common to the early phases of psoriasis development, characterized by cellular players of innate immunity, such as pDC, neutrophils, mast cells, macrophages, and monocytes. In addition, IFN-β and IFN-α2a, two type I IFNs typical of early psoriasis, were highly expressed in paradoxical skin reactions. Concomitantly, other innate immunity molecules, such as the catheledicin LL37 and lymphotoxin (LT)-α and LT-β were overproduced. Interestingly, these innate immunity molecules were abundantly expressed by keratinocytes, in addition to the inflammatory infiltrate. In contrast to classical psoriasis, psoriasiform lesions of HS patients showed a reduced number of IFN-γ and TNF-α-releasing T lymphocytes. On the contrary, IL-22 immunoreactivity was significantly augmented together with the IL-36γ staining in leukocytes infiltrating the dermis. Finally, we found that all HS patients with paradoxical reactions carried allelic variants in genes predisposing to psoriasis. Among them, SNPs in ERAP1, NFKBIZ, and TNFAIP genes and in the HLA-C genomic region were found.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

No result from this study comes from a test of the peptide.

Natural levels measured1

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 01HumanEndogenous levelCase report or seriesMechanism

    In three patients with hidradenitis suppurativa who developed paradoxical psoriasiform reactions on adalimumab, the body's own cathelicidin LL37 was overproduced in the skin lesions.

    In plain wordsIn three patients with skin reactions to adalimumab, the body's own LL37 was overproduced in the affected skin.

    Peptide
    LL-37
    Outcome
    IncreaseLL37 expression in paradoxical psoriasiform reactions
    Study

    n = 3

    Outcome group
    Immune response · Skin and wound

    Source sentences

    Summary
    Concomitantly, other innate immunity molecules, such as the catheledicin LL37 and lymphotoxin (LT)-α and LT-β were overproduced.
    1 context sentence
    Summary · context
    In this study, we investigated the immunological and genetic profiles of three HS patients without psoriasis who developed paradoxical psoriasiform reactions following anti-TNF-α therapy with adalimumab.

    This result measures the body's own LL-37. Nobody was given the peptide. It is not evidence about taking it.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 3Current

    11 Oct 2026, 00:50 UTC

    Study results updated

  2. Version 2

    9 Oct 2026, 03:03 UTC

    Study data updated · source update from Europe PMC

  3. Version 1

    9 Oct 2026, 02:56 UTC

    First added · source update from Europe PMC

Subjects

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