BIO 343 Lecture Notes - Lecture 15: Bcg Vaccine, Tuberculosis, Cell Signaling
Immunology Chapter 15: Types 2,3, and 4 Hypersensitivity
Hayden Casassa
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• Type 2 Hypersensitivity
o Reactions are mediated by IgG made against new epitopes on cell surface proteins
o Cells are subjected to complement activation and phagocytosis, leading to inflammation and
tissue damage
o Diseases assoiated ith Tpe … Penicilin-induced hemolytic anemia, Rheumatic fever, and
Blood transfusion reaction
• Type 2 Hypersensitivity
o IgG is produced against a normal or altered cell surface protein
o Causes damage to cells and tissues
▪ Complement activation
▪ IgG mediated opsonization and phagocytosis
▪ Alteration of cell signalling
o Many autoimmune diseases resemble type 2 hypersensitivity
• Penicilin-induced hemolytic anemia (Type 2)
o Peiilli ids to RBC surfae proteis ad reates e epitopes akig RBC’s antigenic
o Whe odified RBC’s are proessed ad preseted, the atiate CD T ells to eoe TFH
cells helping B cells produce IgG against the new epitope
o Bidig of IgG atiodies to the RBC’s ake the suseptile to opleet-mediated lysis
(MAC) or to phagocytosis in the spleen via complement receptors and Fc receptors
o Causes hemolytic anemia
• Rheumatic Fever is an example of Type 2 hypersensitivity Rx
o Inflammatory autoimmune disorder that develops from complication of Strep
o Individuals have predisposition with certain HLA class 2 genes
• Etiology of Rheumatic fever illustrates Molecular Mimicry (Shown above to right)
o Mechanism that causes autoimmune disease when foreign pathogen shares structural
similarities with host self-proteins
o IgG produced against S. pyogenes cross-react with epitopes on heart and joints causing
complement-induced inflammation and fibrosis
• Why is blood typing important?
o Incompatibilities can cause life-threatening blood transfusion reactions (Type 2)
• Clinical Manifestations of blood transfusion reactions
o Incompatibility causes Type 2 hypersensitivity
o Recipient has preexisting anti-RBC IgG/IgM As that id to door’s RBC ad leads to
complement activation
o Results in RBC lysis and increased levels of toxic billirubin
• A, B, and O antigens are Glycolipids
find more resources at oneclass.com
find more resources at oneclass.com
o Antigens are glycolipids… they are not proteins they’re lipids with sugars
o Chain of oligosaccharides attached to lipid ceramide
o O blood types only have core chain of lipids
o A & B individuals have enzyme called glycosyltransferase that adds additional sugar
o A has extra N-Acetyl galactosamine
o B has extra galactose
o O does’t hae speifi atige ut ore so lak of
A and B antigens
• Individuals with A, B, or O blood have pre-existing Abs against blood antigen they are lacking
o AB has oe… Wh?
o Because we make IgM (or IgG) against commensals that have surface carbohydrates structurally
similar to A and B antigens
▪ Durig B ell deelopet, a A’s that ould reat ith ur o lood tpe u delete
• Rhesus (Rh) antigen
o Highly polymorphic antigen expressed by >85% of population
o Most significant Rh antigen is the D antigen
▪ One is either positive or negative for the antigen
o If you are negative and given positie ou ill aept… ut ill aout iue respose
o If ou are positie ad gie egatie… ou ill aept ith o prole
• Rhesus D antigen reactions
o First time RhD- is gie RhD+… o prole eause e do’t hae pre-existing Abs
o However, second time, anti-RHD Abs generated from 1st reatio ill attak RBC’s
• Type 3 Hypersensitivities
o Caused by immune complexes formed from IgG and soluble antigens that lodge into small blood
vessels or lung alveoli
o Leads to complement activation and extensive inflammation/ tissue damage
o Can occur anytime after large amounts of foreign antigens are injected intraveneously
• Ke for tpe 3 hpersesitiit… Iue ople ith IgG ad solule atiges
• Universal Donor is O→ More so O-
• Universal Recipient is AB → more so AB+
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Immunology chapter 15: types 2,3, and 4 hypersensitivity. Igg is produced against a normal or altered cell surface protein: causes damage to cells and tissues, complement activation, alteration of cell signalling. Igg mediated opsonization and phagocytosis: many autoimmune diseases resemble type 2 hypersensitivity, penicilin-induced hemolytic anemia (type 2) Inflammatory autoimmune disorder that develops from complication of strep. Individuals have predisposition with certain hla class 2 genes: etiology of rheumatic fever illustrates molecular mimicry (shown above to right, mechanism that causes autoimmune disease when foreign pathogen shares structural similarities with host self-proteins. Incompatibilities can cause life-threatening blood transfusion reactions (type 2: clinical manifestations of blood transfusion reactions. If you are negative and given positi(cid:448)e (cid:455)ou (cid:449)ill a(cid:272)(cid:272)ept (cid:271)ut (cid:449)ill a(cid:373)ou(cid:374)t i(cid:373)(cid:373)u(cid:374)e respo(cid:374)se. Initial tb infection (or vaccine) causes clonal expansion of tuberculin-specific th1 memory cells: th1 memory cells continually circulate through skin.
