Adaptive immunity involves various immune cells and molecular mechanisms that together mount an effective primary immune response, whilst establishing an immunological memory that prepares the body for future pathogenic encounters. The process begins with antigen recognition using antigen-presenting cells (APCs) such as dendritic cells and macrophages that are exposed to and engulf pathogens, processing their proteins into antigenic peptides. Such foreign peptides are then presented on the surface of APCs by major histocompatibility complex (MHC) proteins, either class I or class II. Antibody-like T cell receptors (TCRs) on helper T cells (CD4+ cells) interact with antigen-MHC class II complexes, whilst cytotoxic T cells (CD8+) interact with antigen-MHC class I complexes. The interaction between the TCR and the antigenic peptide-MHC complex is further stabilized by interactions between co-receptors on the T-cell surface (CD4 or CD8) and the MHC molecule, enhancing the TCR's binding affinity for the peptide-MHC complex, and triggering T cell activation. Activation of helper T cells involves the binding of the TCR to the antigen-MHC complex, supplemented by co-stimulatory signals from APCs such as B7, and integrins and CD28 on T cells, leading to helper T cell differentiation into specific subsets (Th1, Th2, Th17, Treg) based upon the cytokines present in their microenvironment. B cells that have encountered the same antigen in their specific receptors (B cell receptors or BCRs) are activated but require further signals from helper T cells (Th2 cells) to undergo full development. These B cells also process the antigenic peptides on their MHC class II molecules and activated helper T cells interact with them via the recognition of the antigenic peptide-MHC class II complex by the TCR on the helper T cell. Concurrently, CD40 on the B cell interacts with CD40 ligand (CD40L) on the helper T cell, thereby providing a co-stimulatory signal for B cell proliferation. Cytokines produced by the helper T cells, particularly IL-4, also play an important role in promoting B cell responses. IL-4 promotes class switching in B cells, leading them to change the class of antibodies they produce, for example switching from IgM to producing IgG, IgE, or IgA antibodies, depending on the specific cytokine milieu. Antibodies produced by B cells can neutralize pathogens by binding to their surface antigens, preventing them from infecting host cells or initiating complement activation, leading to the formation of membrane attack complexes (MACs) that lyse pathogens. Finally, antibodies can facilitate phagocytosis through opsonization, marking pathogens for destruction by macrophages and neutrophils. Upon activation, cytotoxic T cells (CD8+) differentiate into effector cells. These cells recognize and destroy infected or abnormal host cells through the release of cytotoxic molecules such as perforin and granzymes, initiating apoptosis in the target cells. Finally, the adaptive immune system generates memory cells during primary immune responses. Memory B cells retain the ability to produce antibodies specific to the encountered antigen, resulting in a faster and stronger secondary immune response upon re-exposure. Memory T cells also develop, enhancing the rapidity and efficacy of the secondary immune reaction. We provide a large product catalogue of research tools for investigating adaptive immunity, including CD45 antibodies, CD4 antibodies, CD3 antibodies, IL10 ELISA Kits, and IL4 ELISA Kits. Explore our full adaptive immunity product range below and discover more, for less. Alternatively, you can explore our T Cells, B Cells, and Regulatory T Cells product ranges.