The role of interleukin (IL)-6 in health and disease has been under a lot of scrutiny in recent years, particularly during the recent COVID-19 pandemic. The inflammatory pathways in which IL-6 is involved are also partly responsible of the development and progression of rheumatoid arthritis (RA), opening interesting perspectives in terms of therapy. Anti-IL-6 drugs are being used with variable degrees of success in other diseases and are being tested in RA. Results have been encouraging, particularly when anti-IL-6 has been used with other drugs, such as metothrexate (MTX). In this review we discuss the main immunologic aspects that make anti-IL-6 a good candidate in RA, but despite the main therapeutic options available to target IL-6, no gold standard treatment has been established so far.

Due to the bivalent nature of DAMP, it is often difficult to explain the relative role of DAMP in inflammation versus its role in tissue repair. However, this point is crucial as DAMP-related treatments move into clinical practice.

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CD4+/CD25+ T cells seem to be impaired in their function during the HAV acute infection. This evidence might help to determine an optimal T helper cell immune network that is a predisposing factor for a self-limiting disease.

Nickel (Ni) inhibits lymphoproliferative responses. Proliferation was performed on PBMC of 20 controls and 10 patients with Ni allergy. NiSO4 was used at a concentration of 0.1mM. PHA was added at a concentration of 5 μg/ml. Cells were incubated for 5 days and proliferation assessed by CFSE staining. At 0.1mM Ni strongly reduced (>40%) PHA-induced proliferation. The inhibition decreases in a dose-dependent manner and response to PHA is restored at 20 mM Ni. Ni alone induces small (<5%) proliferative response in both allergic and non allergic donors. Nickel inhibition requires the presence of Ni in the supernatant and is abrogated when Ni is incubated with the cells for up to 4 hours and the supernatant is washed. Strong inhibition was also observed in preliminary experiments with tuberculin purified protein derivative (PPD) stimulated PBMC. Staining for CD8 on CFSE cultures showed that PHA response was due to both CD8 and CD4 cells. Ni increased % of CD4 cells and decreased the % of CD8 cells. PPD response was predominantly a CD4 response, with Nickel reducing the % of CD4 cells at higher concentations, while unaffecting the CD8. Ni inhibits IL-6 production essential to normal PHA response. The addition of 10–100 IU of IL-6 and/or IL-2 to the cultures did not affect Ni inhibition of PHA proliferation. Addition of IL-6 increased CD25+ cells. Our data suggest that Ni induced inhibition of PHA response is due to steric interference between PHA and its cellular ligand. Further studies will clarify the precise mechanism of Ni mediated inhibition of immune responses and its the role in the pathogenesis of Ni allergy.