Immunity: Humoral and Cellular

The immune system evolved to recognise infectious pathogens. Discrimination between self and nonself is a critical property of the immune system that enables it to eradicate pathogens without harming the host. Immune responses to pathogens are affected initially by the innate immune system, which reacts rapidly to generic pathogen-associated molecules and primes the adaptive immune system, which is slower to react but has exquisite specificity and memory. Here, we outline the spatial framework of the immune system and define its mobile and fixed elements. A range of cell types (including antigen-presenting cells and lymphocytes) and soluble components (including complement, antibody, cytokine and chemokine proteins) circulate and communicate between the bone marrow and lymphoid tissue structures to maintain immune surveillance.

Key Concepts:

  • The immune system is designed to recognise, react to and eradicate ‘nonself’, in particular infectious pathogens.
  • The immune system comprises fixed and mobile elements.
  • The elements of the immune system sequentially mediate innate immunity, providing acute, generic defences and adaptive immunity, providing highly specific, long-lasting defences.
  • The specificity and diversity of adaptive immunity is based on genetic polymorphism of the receptors for antigens on T and B cells and of the major histocompatibility complex (MHC) molecules that bind antigenic peptides recognised by the T-cell receptor.
  • Nonspecific costimulation via surface-interacting molecules or soluble cytokines and chemokines shapes the differentiation of T and B cells in the adaptive immune response.

Keywords: innate; adaptive; MHC; T cell; antibody

Figure 1. Interactions between the antigen-presenting cell (APC) and the T cell. Antigen peptide (Ag) processed by the APC is presented on the major histocompatibility complex (MHC) molecule to the cognate T-cell receptor (TCR). This contact is stabilised by intercellular adhesion molecule (ICAM) 1–leukocyte functional antigen (LFA)-1, LFA-3–CD2 and MHC–CD4 or MHC–CD8 interactions. In addition to stimulation via the highly specific MHC–Ag–TCR interaction, costimulation occurs via B7–CD28. Cytokines secreted by the APC direct T-cell differentiation. Upregulation of CD40 ligand (CD40L) on the T cell further stimulates the APC to present antigen and secrete cytokines. T-cell proliferation is limited by the upregulation of CTLA-4, which inhibits costimulation mediated by CD28. PD-1 and its ligands are members of the CD28/CTLA-4 family of T-cell regulators that have a general effect to negatively regulate T-cell responses.
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 Further Reading
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Harrison, Leonard C, Unglik, Gary, and Honeyman, Margo C(Apr 2010) Immunity: Humoral and Cellular. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1002/9780470015902.a0001236.pub2]