#Shorts 2
How the incident is remembered
- Tissue resident dendritic cells translate and confer the pathogen message to
lymphocytes;
A meshwork of immature dendritic cells resides in a subepithelial layer. They have potent
endocytic and phagocytic activity. Many factors associated with tissue inflammation induces
their maturation and migration into local lymph vessels from there to draining LNs. They
carry and present bacterial Ag from the site of inflammation to a large number of
lymphocytes. Some pathogens may also enter the blood stream. Circulating Ag is taken up
by phagocytic cells, previously known as reticulo-endothelial system (RES) that live within
microvessels in the liver, bone marrow and spleen. The spleen is the major site of
immunisation to blood-borne Ag.
- Stimulation
Short term effects are production of effector T cells (Th1, Th2, CTL) and IgM producing B
cells. While most of these die as soon as the infection is cleared, some Ag-experienced
lymphocytes remain. These memory cells mediate enhanced recall responses upon re-
encounter of the pathogen. Plasma cells generate high affinity circulating antibodies that
neutralize reactive pathogens and/or mark them for rapid phagocytosis.
The adaptive immune system
Mode of action: pathogen-specific humoral and cellular responses; long-lived memory.
Adaptive immunity must deal with pathogens that escape innate immune mechanisms, e.g.
because they hide inside the body’s own cells (e.g. viruses, some bacteria) or because they
are the body’s own cells (e.g. malignant cells or autoreactive lymphocytes; both have no
PAMPs!) or because they have developed resistance to innate effector mechanisms (e.g.
mycobacteria or parasites). These threats to the body’s integrity are recognized because
they generate non-self molecular patterns, i.e. antigens. Lymphocytes recognize Ag by virtue
of their unique Ag receptor, which recognize structural features of foreign peptides or lipids
presented in the context of MHC molecules or CD1, respectively.
Lymphocyte honing
A few simple rules (which have exceptions): - every lymphocyte has exactly one Ag receptor,
which recognizes a unique “cognate” non-self Ag; - naïve lymphocytes are stimulated by Ag
only when it is encountered on the surface of professional APC together with appropriate
costimulation;
See full - HST 175 (mit.edu)
How the incident is remembered
- Tissue resident dendritic cells translate and confer the pathogen message to
lymphocytes;
A meshwork of immature dendritic cells resides in a subepithelial layer. They have potent
endocytic and phagocytic activity. Many factors associated with tissue inflammation induces
their maturation and migration into local lymph vessels from there to draining LNs. They
carry and present bacterial Ag from the site of inflammation to a large number of
lymphocytes. Some pathogens may also enter the blood stream. Circulating Ag is taken up
by phagocytic cells, previously known as reticulo-endothelial system (RES) that live within
microvessels in the liver, bone marrow and spleen. The spleen is the major site of
immunisation to blood-borne Ag.
- Stimulation
Short term effects are production of effector T cells (Th1, Th2, CTL) and IgM producing B
cells. While most of these die as soon as the infection is cleared, some Ag-experienced
lymphocytes remain. These memory cells mediate enhanced recall responses upon re-
encounter of the pathogen. Plasma cells generate high affinity circulating antibodies that
neutralize reactive pathogens and/or mark them for rapid phagocytosis.
The adaptive immune system
Mode of action: pathogen-specific humoral and cellular responses; long-lived memory.
Adaptive immunity must deal with pathogens that escape innate immune mechanisms, e.g.
because they hide inside the body’s own cells (e.g. viruses, some bacteria) or because they
are the body’s own cells (e.g. malignant cells or autoreactive lymphocytes; both have no
PAMPs!) or because they have developed resistance to innate effector mechanisms (e.g.
mycobacteria or parasites). These threats to the body’s integrity are recognized because
they generate non-self molecular patterns, i.e. antigens. Lymphocytes recognize Ag by virtue
of their unique Ag receptor, which recognize structural features of foreign peptides or lipids
presented in the context of MHC molecules or CD1, respectively.
Lymphocyte honing
A few simple rules (which have exceptions): - every lymphocyte has exactly one Ag receptor,
which recognizes a unique “cognate” non-self Ag; - naïve lymphocytes are stimulated by Ag
only when it is encountered on the surface of professional APC together with appropriate
costimulation;
See full - HST 175 (mit.edu)
