Immunology Flashcards
FasR (CD95)
Apoptosis of T cells (CD 4 and CD8)
Primary signal of CD8 activation
TCR of naive T cell specific for Ag binds peptide on MHC I on DC.
Secondary signal of CD8 response
B7 costimulatory molecule on APC binds to CD28 on T cell, then T cell becomes activated cytotoxic T cells (CTL)
Colonal expansion of T cells
CD8 T cell secretes cytokines IL-2
CTLs also secrete perforins and granzymes
Then go to infected tissue
Activated CD4 cells release
Th0
Th0 can develop into the following Th cells:
Th1, Th2, Tfh
Th0 (DC) cells activate into _______ in the presence of _______ and then activate Macrophages by expressing ________
Th1, IL12, CD40L to CD40 on MO and IFN-gamma to IFN-gammaR on MO causing MO to produce NO and oxygen radicals and TNF, IL-1
Intravesicular bacteria
Th2 and Tfh activation
Soluble and extracellular Ag
DC ingested Ag presents in lymph on MHC II as peptide to activate naive T cells
B cells phagocytosis ECM Ag in lymph node and present peptide on MHC II
Two signals for CD 4 activation from Th2 and Tfh in lymph node
In presence of IL-4 CD4 differentiates into Th2 or Tfh, which then bind to Ag presenting B cells
Th2 binds CD40L to CD40R on Bcell
Th2 secrete IL-4,IL-5 which induce B cell proliferation and differentiation into IgM plasma cells and somatic hyper mutation and isotope switching to IgE
Tfh cells secrete _______ during Th0 activation
IL-21, IL-4, IFN-gamma
Tfh induces B cells to undergo isotype switching and somatic hypermutation to isotopes other than IgE
Affinity Maturation
Colonial selection as Ag levels drop bc of Ag clearance,resulting in B cell survival with the highest Ag binding affinity and will have an isotype other than IgM (which are short lived plasma cells)
After activation, each B cell will have Ab with one specificity and one isotype expressed
CD40R deficiency
Hyper-IgM syndrome
Lack of isotype switched Ab but abundance of IgM
Toll-like receptors
Recognize structurally conserved molecules derived from microbes (PAMPs)
The TLR triggered determines what cytokines DC secrete
Haptens
Non-immunogenic foreign substances that can react with an Ab on a B cell, trigger an immune response when coupled to a carrier protein
I.e. Urushiol –> poison ivy, reacts w skin proteins and forms hapten conjugates to induce an immune response
I.e. Conjugate vaccine
Opsonization
Pathogen is marked for ingestion and is phagocytosed.
Complement steps
Inflammation
Opsonization
Lysis of bacteria
Occurs in classical and alternative complement pathways
Classical pathway triggered by
Binding of IgM or most IgG isotypes to a pathogen
Activated C1 acts on C2 and C4 and cleaves C4 into C4a and C4b
C3 convertase C4b2b cleaves C3 into C3a and C3b
Best opsonin is:
best inflammatory one:
C3b
C5a
MAC membrane attack complex:
C5b6-9
Alternative pathway
More innate, can activate without Ab
C3b spontaneously cleared by C3, same MAC
what are the two ways natural killer cells can Kill their target
1) via antibody dependent cellular cytotoxicity (ADCC) with the aid of antibodies
NK cell binds to IgGs Fc portion with its Fc receptor and NK secretes granzyme and perforins
2) natural killer cells can cause death and target cells that expressed a lack of an MHC 1 expression
Via KIR (killer inhibitory receptor) that recognizes MHC I
What antibody process of Placenta during pregnancy
IgG, which protect the baby, and is present and the newborn immediately after birth known as passive immunity
Low count of antibodies between three and six months
IgM is produced in utero and has about 50% at birth
Type I Hypersensitivity
Immune initiator
Ag type
Rxn Mechanism
Ex
Immediate
IgE and mast cells which release toxic mediators (usually the result of symptoms)
Soluble Ag
Mast cell activation
Allergic, asthma
Mechanism: sensitization (like Th2 response), activation (immediate, seconds and late, hours)
Skin test
Type II Hypersensitivity
Immune initiator
Ag type
Rxn Mechanism
Ex
IgG
Cell mediated or matrix Ag
Complement (MAC), FcR cells (MO and NK cells)
Drug allergins
Foreign induced example: drugs, blood transfusion, graft rejection
Autoantigen induced example: myasthenia gravis, Graves’ disease, autoimmune hemolytic disease
Type III Hypersensitivity
Immune initiator
Ag type
Rxn Mechanism
Ex
IgG
Soluble Ag
Complement, Phagocytes, Inflammation
Localized foreign Ag-induced example: Arthur’s rxn
Generalized foreign Ag-induced rxn: Serum sickness
Generalized autoAg induced: rheumatoid arthritis, lupus (butterfly rash)
Type IV Hypersensitivity
Immune initiator
Ag type
Rxn Mechanism
Ex
Delayed type, 48-72hrs
Th1 and CTL (cytotoxic T cell lymphocytes)
Soluble Ag and cell associated Ag
MO and Cytotoxicity via CTL
Contact dermatitis and graft rejection
ForeignAg induced examples: poison ivy, PPD test, chronic allograft rejection
AutoAg induced Rxns example: type I diabetes, multiple sclerosis
CTLA-4
Down regulates T cells (CD 4 and CD 8)
