Interleukin 1 delta Proteins (FIL1d)

Mouse (Murine) Interleukin 1 delta (FIL1d) interaction partners

1. these data reveal that IL-1Ra and IL-36Ra have opposing effects on the outcome of Pseudomonas aeruginosa keratitis

2. IL-36 promotes myeloid cell infiltration, activation, and inflammatory activity in skin

3. Interleukin-36 (IL-36) ligands require processing for full agonist (IL-36alpha, IL-36beta, and IL-36gamma) or antagonist (IL-36Ra) activity

4. Transcripts for IL-1F5 are significantly increased in the involved skin of bi- and monotransgenic mice compared with their C57BL controls.

5. IL-1F5 has unique loop conformations for receptor binding specificity

6. IL-1F5 mediates anti-inflammatory effects through its ability to induce interleukin-4 production, as a consequence of its interaction with orphan receptor single Ig IL-1R-related molecule (SIGIRR)/TIR8.

Human Interleukin 1 delta (FIL1d) interaction partners

1. The IL36RN gene mutation is not a constant condition in drug-induced AGEP.

2. The results show, significant correlation of IL36RN mutations with a younger age at psoriasis onset. Psoriasis patients with IL36RN mutations, carried an additional rare variant in either CARD14 or AP1S3, indicating a more complex inheritance.

3. Letter/Case Report: generalized pustular psoriasis and geographic tongue had a heterozygous IL36RN mutation and IgG2 deficiency.

4. IL36RN may be the most common disease-causing gene in the patients with generalized pustular psoriasis in the Han population from Sichuan region.

5. systemic lupus erythematosus patients had significantly decreased serum IL-36Ra levels

6. IL36RN may be the major disease-causing gene in generalized pustular psoriasis patients in Han population in Sichuan region of China.

7. IL36RN mutations were strongly linked with early onset and hyponychial pustules, but not with therapeutic efficacy of acitretin or recurrence frequency. Early onset and hyponychial pustules may be specific to IL36RN mutation, however this alone is an insufficient biomarker for acitretin therapy.

8. Using different blood leukocyte and skin resident cell preparations, and recombinant proteins, the authors have identified that neutrophil elastase, but not other neutrophil derived proteases, cleaves IL-36Ra into its highly active antagonistic form.

9. A study on the association of IL36RN mutations that affect protein expression and function with phenotype in patients with generalized pustular psoriasis.

10. The findings indicate that IL36RN mutations do not seem to contribute to the pathogenesis of common, nonpustular forms of psoriasis, but to the rarer pustular manifestations such as GPP, acrodermatitis continua suppurativa of Hallopeau and acute generalized exanthematous pustulosis.

11. Some cases of geographic tongue are caused by IL36RN mutations, while those lacking mutations are associated with an imbalance in expression between IL-36Ra and IL-36gamma proteins in tongue tissue.

12. Study data and the previous European study suggest that palmoplantar pustulosis is not associated with mutations of the IL36RN gene.

13. Case Report: short-term infliximab for treatment of juvenile generalized pustular psoriasis with IL36RN mutation.

14. The authors present a case of strikingly distinct phenotypes seen in two IL36RN mutation carriers from the same nonconsanguineous pedigree. This mutation it appears may influence the age of onset.

15. The present study identified IL-36RN in various species and investigated the associations between IL-36RN and cancer prognosis.

16. We identified a novel homozygous missense mutation in IL36RN in two siblings, and showed the molecular basis of the condition to be both distinct from psoriasis and distinct between the two families studied.

17. generalized pustular psoriasis and early onset, ever generalized pustular psoriasis (more than two attacks), ever acrodermatitis continua of Hallopeau, inverse psoriasis, and a family history of pustular psoriasis were associated with IL36RN mutation.

18. IL36RN was identified as strong regulators of skin pathology in both lesional and non-lesional skin samples.

19. IL36RN missense mutation was not associated with psoriasis.

20. we report T123M and 115+6T>C mutations, both homozygous in nature, in two Japanese individuals with Zumbusch type of generalized pustular psoriasis.