Immunity II Flashcards
what is immunologic tolerancr
-lack of response to antigens that is induced by exposure of lymphocytes to these antigens
- ability to discriminate between self and nonself antigens
normally microbes are:
- self antigens are:
immunogenic; tolerogenic
what is central tolerance
developing lymphocytes encounter self antigens in central lymphoid organs
what is peripheral tolerance
mature lymphocytes encounter self antigens in peripheral tissues
what do self reactive T cells do in central T cell tolerance
- negative selection or deletion
- development of regulatory T cells
what do regulatory T cells do in peripheral T cell tolerance
block the activation of self reactive lymphocytes
what is anergy
functional inactivation of T cells
what is deletion
apoptosis of self reactive lymphocytes
what induced tolerance in B cells
self polysaccharides, lipids and nucleic acids
what does central B cell tolerance undergo
- receptor editing
- negative selection
what does peripheral B cell tolerance undergo
- anergy
- excluded from lymphoid follicles
what is autoimmunity
immune response against self antigens
what might the development of autoimmunity be due to
- inheritance of susceptibility genes
- environmental triggers
most autoimmune diseases are______
polygenic
what are autoimmune diseases often associated with
particular HLA genes that are inefficient at displaying self antigens
- defective T cell negative selection
- may fail to stimulate regulatory T cells
how might infections activate self reactive lymphocytes
-increased production of costimulatory molecules on APCs
- molecular mimicry
what are hypersensitivity reactions
injurious or pathologic immune reactions
what is autoimmunity
- reactions against self antigens
- failure of self tolerance
what does hypersensitivity cause
- autoimmunity
- reactions against microbes
- reactions against environmental antigens
describe type I immediate hypersensitivity
- tissue reaction that occurs rapidly after interaction of antigen with IgE antibody bound to mast cell
- often develop in atopic individuals
- environmental and food allergens
- mild to severe reaction
what is the mechanism of type 1 immediate hypersensitivity
- activation of Th2 cells and IgE class switching in B cells
- production of IgE
- binding of IgE to Fc on mast cells
- repeat exposure to allergen
- activation of mast cell and release of mediators
- mediators could be vasoactive amines or cytokines
- vasoactive amines cause immediate hypersensitivity reaction
- cytokines cause late phase reaction
what is an example of a vasoactive amine and what does it do
histamine: causes vasodilation, increased vascular permeability, smooth muscle contraction and increased secretion of mucus
what are the lipid mediators and what do they cause
- prostaglandins and leukotrienes: smooth muscle contraction and vascular permeability
what are the cytokines released in immediate hypersensitivity
TNF, chemokines, Il4 and IL5
what are the clinical syndromes and manifestations of type I immediate hypersensitivity reactions
- anaphylaxis: fall in BP, vascular dilation, airway obstruction due to laryngeal edema
- bronchial asthma: airway obstruction due to smooth muscle hyperactivity
- allergic rhinitis: increased mucus secretion, inflammation of upper airways and sinuses
- food allergies: increased peristalsis causes vomiting and diarrhea
how do allergies develop
- genetically determined
- environmental factors: environmental pollutants, infections
- atopic individuals