When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.

Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for activating CD8 cells. The dendritic cells present antigens with MHC I to CD8 cells, and the Th1 cells secrete cytokines, which activate and differentiate CD8 cells into cytotoxic T cells, responsible for recognizing and destroying virus-infected or cancerous cells. Additionally, Th1 effector cells secrete cytokines that activate macrophages, essential for cell-mediated immunity.

On the other hand, Th2 effector cells secrete cytokines like IL-4 that act as co-stimulatory molecules for the activation of B cells. These cells directly interact with B cells with specific antigen fragments bound to class II MHC receptors. When a Th2 cell binds to a B cell, it releases cytokines that stimulate the B cells to divide more rapidly. This process continues as long as the Th2 stimulation persists. The Th2 cell then signals for the production of antibodies, activating B cells to unleash their protective potential. Some B cells can be activated by T cell-independent antigens. However, such antigens tend to elicit weak and short-lived responses. Most antigens are T cell-dependent antigens that require T cell help to activate the B cells to which they bind.

Other cytokines like IL-5, secreted by Th2 cells, mobilize eosinophils, which assist in worm infections and allergies.

Similarly, IL-17 is a pro-inflammatory cytokine produced primarily by Th17 cells. It is crucial in inflammatory reactions against extracellular microbes and autoimmune diseases, including multiple sclerosis. IL-17 helps recruit and activate neutrophils and other immune cells at infection sites, boosting the production of pro-inflammatory cytokines and chemokines to clear pathogens. Also, IL-17 is implicated in the pathogenesis of autoimmune diseases, for example in multiple sclerosis (MS), it contributes to the inflammatory environment that damages myelin and nerve fibers in patients with MS. In rheumatoid arthritis, IL-17 contributes to chronic inflammation and joint destruction in RA by promoting the production of pro-inflammatory cytokines, matrix metalloproteinases, and other mediators that lead to cartilage degradation and bone erosion. In psoriasis, IL-17 promotes the proliferation of keratinocytes and the production of inflammatory mediators, involved in the development of psoriatic skin lesions.

Finally, T regulatory cells are a subset of T helper cells that suppress self-reactive lymphocytes outside the lymphoid organs, preventing autoimmune diseases. T regulatory cells dampen the immune response by direct contact or by releasing inhibitory cytokines.