To show the reduction in Mys expression was due to relocalization, we examined the total cellular antibody-bound pool by staining permeabilized cells for Mys.
Quadrants of dot plot were set using appropriate isotype controls for each intra- and extra-cellular antibody.
As such, the term anti-cellular antibodies has been suggested to encompass the wider spectrum of these autoantibodies [8, 9].
The presence of anti-cellular antibodies [1], commonly referred to as antinuclear antibodies (ANA), directed against intracellular antigens is a hallmark of ANA-associated rheumatic diseases (AARD) [2].
Mean fluorescent intensity of cell surface antibodies and intra-cellular antibodies were obtained from FlowJo software (Treestar).
Currently, the majority of approved therapeutic antibodies are of the human IgG1 format, which productively engages immune effector functions (e.g., antibody-dependent cellular cytotoxicity, antibody-dependent cellular phagocytosis, and complement-dependent cytotoxicity).
At present, the majority of approved therapeutic antibodies are of the human IgG1 format, which can elicit immune effector functions (e.g., antibody-dependent cellular cytotoxicity, antibody-dependent cellular phagocytosis, and complement-dependent cytotoxicity).
The main biological functions of antibodies are neutralization, complement activation, cellular cytotoxicity antibody dependent, and opsonization.
Both C5 deficiency and the systemic administration of anti-C5 antibodies ameliorated CIA, whereas both cellular and antibody responses to immunization with collagen II were normal [ 23, 27].
Despite these advances, significant challenges remain in the identification of optimal cellular targets, antibody forms and treatment schedules for therapeutic applications.
