Differential Expression of CD30 on CD3 T Lymphocytes in Patients with Systemic Lupus Erythematosus

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune systemic disease caused as a result of an imbalance of Th1-/Th2-type cytokines. The soluble form of CD30 (CD30s) released from peripheral blood cells has been described as a marker of active disease in Th2-type immune response as in SLE. However, the expression of CD30 on CD3 T lymphocytes from patients with SLE has not been studied yet. Therefore, we have addressed our study to attempt this issue, studying CD30 expression by flow cytometry on CD3 T lymphocytes and CD4/CD8 subsets in samples from SLE patients mainly with lupus nephritis. In parallel, we have determined the production of the cytokines IL-4 (Th2), IFNc (Th1), IL-10 and TGFb by intracellular staining. Differences between positive CD30 T cells in healthy controls and patients with SLE were found, with a higher percentage of CD30-expressing T cells in patients with SLE (P = 0.001). In contrast to healthy controls, CD30 was mainly expressed on CD8 T cells from patients with SLE. The intracellular cytokine staining showed that TGFb is the main cytokine expressed in CD3 T cells from patients with SLE. In addition to this, we have found a positive correlation between CD30-expressing T cells and IL-4, IFNc, and immunosuppressive cytokines (IL-10 and TGFb) (P < 0.05). These results suggest that CD30 could play a role in the pathogenesis of SLE and its expression on CD3 T lymphocytes is not restricted only to Th2-type response.

CD30 expression and survival in extranodal NK/T-cell lymphoma: a systematic review and meta-analysis

“…Inflammation from EBV infection which has also been observed as a cause of the CD30 expression in bystander neoplastic cells and elevated soluble CD30 [ 14 ]. This description has been also supported by other studies investigating inflammatory disorders such as systemic lupus erythematosus and inflammatory bowel disease [ 17 , 18 ]. That might be why the effect of the CD30 expression is more obvious among studies included participants predominant in the early stage.…”

Abnormal Interactions between Perifollicular Mast Cells and CD8+ T-Cells May Contribute to the Pathogenesis of Alopecia Areata

“…Next, we also performed triple-IHC for CD30L, since its expression by MCs is up-regulated under pro-inflammatory conditions [86]–[88]; moreover, activated CD8+ T-cells can express CD30 which is implicated in the control of CD8+ T-cell proliferation and cytokine production [83], [85], [89]–[91]. Figure 4M–S shows that the total number and percentage of CD30L+ MCs was significantly up-regulated in lesional AA skin compared to healthy and non-lesional human skin ( Figure 4Q,S ).…”

Autologous T Cells Expressing CD30 Chimeric Antigen Receptors for Relapsed or Refractory Hodgkin Lymphoma: An Open-Label Phase I Trial

“…Although the reason and mechanism of the local anaphylaxis we observed are unclear as of now, Maus and colleagues first reported clinical anaphylaxis resulting from CAR-modified T cells and suggested that anaphylaxis was most likely triggered by an IgE antibody specific for the murine-based antibody sequences present in the CAR-modified T-cell product (16). As the expression of CD30 in normal tissues identified a rare population of large lymphoid cells in sections of lymph node, tonsil, thymus, and endometrial cells with decidual changes (4,17,18), it may be one interpretation of CART-30 cell therapy without significant on-target, off-tumor toxicities.…”