Table 2.
Authorship | Articles Title | Findings |
---|---|---|
Charles et al. [41] | Basophils and the T-helper 2 environment can promote the development of lupus nephritis | In SLE, the presence of elevated serum IgE, self-reactive IgE, and activated CD62L+ and HLA-DR+ basophils are associated with active lupus nephritis and correlate with disease severity. |
Dema et al. [44] |
Immunoglobulin E plays an immunoregulatory role in lupus | The autoreactive IgE in SLE patients is associated with basophil activation and correlates with disease severity. |
Liang et al. [45] |
Basophil count, a marker for disease activity in systemic lupus erythematosus. | Different basophil counts in patients with active and nonactive disease, respectively. |
Dijkstra. [46] |
Human basophils modulate plasma cell differentiation and maturation | Basophils intensify proliferation and class switching in B-cell differentiation into plasma cells and production of immunoglobulins. |
Pan et al. [42] |
Basophil Activation-Dependent Autoantibody and Interleukin-17 Production Exacerbate Systemic Lupus Erythematosus | The presence of autoreactive IgE can mediate basophil activation in SLE. Basophils can amplify autoantibody production by B cells and promote Th17 differentiation. |
Liang et al. [47] |
Low level of circulating basophil counts in biopsy-proven active lupus nephritis | Prognostic value of basophil count in lupus nephritis. |
Pellefigues et al. [48] |
Prostaglandin D2 amplifies lupus disease through basophil accumulation in lymphoid organs | SLE patients have increased expression of PTGDR on basophils and elevated PGD2 metabolites. |
Hasni et al. [49] |
Safety and tolerability of omalizumab: A randomized clinical trial of humanized anti-IgE monoclonal antibody in systemic lupus erythematosus. | Omalizumab may improve SLE activity by decreasing IFN-I production and impairing pDC and basophil activation. |