Humoral mediators for adaptive immunity are the famous immunoglobulins
whose subtypes are IgM, IgG, IgA and IgE. Once stimulated by the intruding
foreign materials (or organisms), APC process and present antigens with MHC II to
immature CD4+ T helper cells to let these cells become effector Th1 or Th2 cells to
help B cells to differentiate into plasma cells. At initial phase of antigen exposure,
low affinity plasma cells produce multivalent IgM, which bind antigens with high
avidity. Some plasma cells produce high-affinity IgG after class switch recombination, and somatic hypermutation and affinity maturation in germinal center. IgM
and IgG make immune complexes that will be cleared by complement system in the
blood or by tissue-resident macrophages. Th1 pathway is considered to be mainly in
charge of defending intracellular bacteria or protozoa, and Th2 pathway in charge
of defending extracellular parasites including helminth. IgA is just the secretary
type and working mainly in mucosal surfaces such as intestinal mucus layers.
21.2 Recent Updates of Innate and Adaptive Immunity
Innate and adaptive immune responses have been considered to have characteristic
discernable features from each other in terms of specificity of response, trainability
of response strength [3], source of the cells involved, and memory capability [1].
However, the recent development of molecular mechanistic scrutiny revealed that
the differences are not clear-cut and there is a spectrum of the responses [1]. This is
also the case with the characterization of the cells involved in both types of immune
responses. The cells of interest are monocyte/macrophages of innate immunity and
T cells of adaptive immunity.
Firstly, specificity of response is prominent in T helper/B cells (and associated
Ig’s) and moderate in cytotoxic T cells (and associated TCRs) and very low in
monocytes and macrophages (almost nonspecific). Dendritic cells are involved to
present antigens to both T helper cells and cytotoxic T cells and there is an overlap
in their function with macrophages and monocytes [12]. Specificity should be
considered not in terms of dichotomous characteristics of innate or adaptive
immunity but as a spectrum from specific, cross-reactive, not-so-selective, changing
along time, or persistently non-specific.
Secondly, trainability of response strength was once thought to be the characteristic feature of adaptive immunity, however, recent discovery of trained innate
immunity cast a challenge that trainability should not be the criteria to discern
adaptive immunity from innate immunity [3]. Response strength of innate immunity
came to be higher at the second challenge of invading organism. Epigenetic
modification of the cells in charge of innate immunity is now considered to cause
this phenomenon [3]. Obviously, cellular and humoral adaptive immunity shows
brisk and higher immune response to the second challenge of invading foreign
materials. This trained response is associated with the memory of effector T cells
consisting of helper T cells in humoral response and cytotoxic T cells in cellular
response.
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whose subtypes are IgM, IgG, IgA and IgE. Once stimulated by the intruding
foreign materials (or organisms), APC process and present antigens with MHC II to
immature CD4+ T helper cells to let these cells become effector Th1 or Th2 cells to
help B cells to differentiate into plasma cells. At initial phase of antigen exposure,
low affinity plasma cells produce multivalent IgM, which bind antigens with high
avidity. Some plasma cells produce high-affinity IgG after class switch recombination, and somatic hypermutation and affinity maturation in germinal center. IgM
and IgG make immune complexes that will be cleared by complement system in the
blood or by tissue-resident macrophages. Th1 pathway is considered to be mainly in
charge of defending intracellular bacteria or protozoa, and Th2 pathway in charge
of defending extracellular parasites including helminth. IgA is just the secretary
type and working mainly in mucosal surfaces such as intestinal mucus layers.
21.2 Recent Updates of Innate and Adaptive Immunity
Innate and adaptive immune responses have been considered to have characteristic
discernable features from each other in terms of specificity of response, trainability
of response strength [3], source of the cells involved, and memory capability [1].
However, the recent development of molecular mechanistic scrutiny revealed that
the differences are not clear-cut and there is a spectrum of the responses [1]. This is
also the case with the characterization of the cells involved in both types of immune
responses. The cells of interest are monocyte/macrophages of innate immunity and
T cells of adaptive immunity.
Firstly, specificity of response is prominent in T helper/B cells (and associated
Ig’s) and moderate in cytotoxic T cells (and associated TCRs) and very low in
monocytes and macrophages (almost nonspecific). Dendritic cells are involved to
present antigens to both T helper cells and cytotoxic T cells and there is an overlap
in their function with macrophages and monocytes [12]. Specificity should be
considered not in terms of dichotomous characteristics of innate or adaptive
immunity but as a spectrum from specific, cross-reactive, not-so-selective, changing
along time, or persistently non-specific.
Secondly, trainability of response strength was once thought to be the characteristic feature of adaptive immunity, however, recent discovery of trained innate
immunity cast a challenge that trainability should not be the criteria to discern
adaptive immunity from innate immunity [3]. Response strength of innate immunity
came to be higher at the second challenge of invading organism. Epigenetic
modification of the cells in charge of innate immunity is now considered to cause
this phenomenon [3]. Obviously, cellular and humoral adaptive immunity shows
brisk and higher immune response to the second challenge of invading foreign
materials. This trained response is associated with the memory of effector T cells
consisting of helper T cells in humoral response and cytotoxic T cells in cellular
response.
392
D. S. Lee and Y. K. Shin