Immunity 1 Flashcards
-A substance that can induce an immune response when introduced into an animal.
Antigen (Ag)
-A protein that is produced in response an antigen. It binds the antigen that stimulated its production. All are immunoglobulins.
Antibody (Ab)
-A glycoprotein composed of heavy and light chains that can function as an antibody.
Immunoglobulin (Ig)
•First immunoglobulin to appear in an immune response
IgM
- Principal immunoglobulin of the secondary immune response
* Only immunoglobulin capable of crossing the placental barrier
IgG
•Principal immunoglobulin in mucosal secretions (ie. tears, saliva) and breast milk
IgA
•-plays an important role in immediate hypersensitivity reactions and parasitic infections•Low concentrations in circulation•Bound to tissue mast cells
IgE
- -thought to activate the B-lymphocyte
- Expressed on B cells
- Not secreted
IgD
Only ____ undergo gene rearrangement
Lymphocyte
When there is class switching of antibodies, what portion of the Ig is changed?
Constant region
- X-linked genetic disease: more common in males
- A primary immunodeficiency disease
- Can’t make antibody and are deficient in opsonization(primary function of antibody)
- Recurrent bacterial infections
- Treatment: intravenous infusions of immunoglobulin every 3-4 weeks for life (passive immunity)
X-linked Agammaglobulinemia
Group of primary immune deficiency disorders Defective class switching Elevated IgM levels; low levels of IgG, IgE, IgA
Hyper IgM Syndromes
Antibodies are produced by which cell? A Macrophage B Mast Cell C T lymphocyte D B lymphocyte E Neutrophil
B Lymphocyte
Which is the first antibody to appear in an immune response? AIgG BIgM CIgA DIgE
IgM
Which is the antibody found in external secretions?
IgA
All lymphocytes arise in the ______
bone marrow
•_____ lymphoid organs–Bone marrow–Thymus
Primary
_____ lymphoid organs–Lymph nodes–Tonsils–Spleen–Mucosal-associated lymphoid tissue (MALT)
Secondary
B lymphocytes become _____ and secrete antibodies when challenged by antigen
plasma cells
Where do T cells become educated and learn self from non-self; self-reacting t cells are deleted
Thymus
_____ cells kill virus infected and damaged cells
CD8 T cells
____ cells help cytotoxic T cells and B cells in their immune functions
CD4 T cells
_____ cells produce antibodies
B Cells
Both _____ and _______ can be found near an infection
-The interaction between these cells is important in eliminating infection.
macrophages and lymphocytes
–A component of the innate immune system
–A type of cytotoxic lymphocyte
–Do not have markers for B or T cells
Natural Killer cells
–CD4+ (T Helper Cell) –quarterback
–CD8+( Cytotoxic T Cell) –effector
–Cell-mediated defense against intracellular pathogens
•Viruses, fungi and bacterial disease (tuberculosis)
•T lymphocytes
B lymphocytes leave the ________ and populate lymph nodes
bone marrow
T lymphocytes leave the ______ and populate lymph nodes
thymus
Are intracellular pathogens dealt with using cellular or humoral immunity?
Cellular immunity
Are extracellular pathogens dealt with using cellular or humoral immunity?
Humoral immunity
_____ immunity
–Early
–Physical and chemical barriers: epithelium and antimicrobial substances
–All phagocytic cells: neutrophils, macrophages, NK cells
–Complement proteins
–Cytokines: TNF, IL-1, interferon
Innate immunity
\_\_\_\_\_ immunity –Later –Antibodies –Lymphocytes –Cytokines (IL-2, IL-12)
Adaptive immunity
_______
–First line of defense against extracellular pathogens
–Antibody dependant
Humoral immunity
______
–First line of defense against intracellular pathogens
–Antibody independent
Cellular immunity
What is the critical step in the complement system?
Cleavage of C3
- Originally discovered on leukocytes and called Human Leukocyte Antigens (HLA)
- All cells of the body have these molecules
- These molecules are recognition molecules that allow the immune system to distinguish self from non-self
MHC molecules
- The recognition arm of cellular immunity –the “bloodhounds”
- Role is to look at all the MHC-2 molecules in the body (on APCs) to determine if they’re “clean” or “dirty”
CD4+ T Helper Lymphocyte
CD4+ T helper cells secretes what cytokine that signals naïve lymphocytes to differentiate into CD8+ Cytotoxic lymphocytes?
IL-2
- The effector arm of cellular immunity
- Role is to scout the body for dirty MHC-1 molecules on somatic cells and kill them
- AKA: Cytolytic T-cells, Killer T cells, Cytotoxic lymphocytes, CTL
CD8 Killer T cells
CD8 Killer T-Lymphocytes kills hepatocyte via ______, exposing virus to humoral immune system
perforins
______ are recognition molecules that allow the immune system to distinguish self from non-self.
MHC molecules
Defects in \_\_\_\_\_\_\_\_ immunity •Bruton X-linked agammaglobulinemia •IgA deficiency •Hyper IgM syndrome •Common variable immune deficiency (CVID)
humoral immunity
Defects in \_\_\_\_ immunity •DiGeorge syndrome •Bare lymphocyte syndrome •Severe combined immunodeficiency (SCID) •Acquired immunodeficiency syndrome (AIDS)
cellular immunity
- Failure of B cell maturation to plasma cells
- No plasma cells
- No antibodies
- Recurrent bacterial infections
- X-linked inheritance: affects only males–Lyonization
Bruton X-Linked Agammaglobulinemia - XLA
- Common immune deficiency (1:700)
- Defect in differentiation of IgA secreting plasma cells
- Low levels of circulating and secretory IgA
- Low morbidity
- Recurring infections of respiratory and gastrointestinal tracts
IgA deficiency
- Defect in class switching from IgM to IgG and IgA antibody production
- High levels of IgM
- No IgG or IgA
- Recurring bacterial infections
- X-linked inheritance
Hyper IgM syndrome
- Common primary immunodeficiency
- A heterogenous group of 20–30 immunodeficiencies
- Symptoms: all exhibit hypogammaglobulinemia due to different causes
- Recurring bacterial infections
- Treatment: intravenous infusion of immunoglobulins
Common Variable Immune Deficiency (CVID)
- Congenital absence of structures derived from the 3rd and 4th branchial pouches
- Thymic and parathyroid aplasia
- No cellular immunity -no T Cells (neither CD4 nor CD8)
- Hypoparathyroidism
- Defects in humoral immunity
DiGeorge Syndrome - Thymic Aplasia
______
APC don’t express MHC Class II molecules
Bare Lymphocyte Syndrome
- A heterogenous group of diseases caused by defective development of both T and B cells
- No T cells
- No B cells
- No humoral and cellular immunity -lethal
Severe Combined Immune Deficiency (SCID)
•HIV ______ is a perfect fit for the CD4 receptor on T cells
gp 120
•HIV _______ promotes fusion
gp 41
- As CD4 cells are killed, cellular immunity fails, followed by humoral immunity
- Infections by intracellular pathogens as cellular immunity fails
- Infections by extracellular pathogens as humoral immunity fails
- Neoplasms
HIV/AIDS
- Aphthous ulcers
- Candidiasis
- Human papilloma virus lesions -papillomas
- Herpes simplex virus lesions
- Hairy leukoplakia (Epstein Barr virus)
- Accelerated periodontitis
- Necrotizing ulcerative gingivitis, periodontitis, stomatitis
- Kaposi sarcoma (HHV-8)
- Other Neoplasms (squamous cell carcinoma, lymphoma)
Oral lesions in ______
Defects in _______:
•Abnormalities in leukocyte adhesion molecules(LFA-1 and MAC-1)
•Defect in actin molecules(lazy leukocytes)
•Defects in microtubule assembly(Chediak-Higashi)
•Defect in NADPH oxidase(Chronic granulomatous disease of childhood)
•Myeloperoxidase deficiency
* Diabetes mellitus
Leukocytes defects
- Advanced periodontitis
- Early loss of primary teeth
- Palmar-plantar hyperkeratosis
- Mutations of the Cathepsin C gene
- Autosomal recessive inheritance
Papillon Lefevre Syndrome
–Immediate Hypersensitivity
–Type I hypersensitivity
–Type ____immune injury –Antibody-Mediated Hypersensitivity
Type 2 hypersensitivity
–Type ___ immune injury –Immune Complex-Mediated Hypersensitivity
Type 3 hypersensitivity
–Type___ immune injury –Cell-Mediated Hypersensitivity
Type 4 hypersensitivity
•Type ____ hypersensitivity –FAST: immediate hypersensitivity–hives in 10 minutes secondary to antigen exposure–Mediated by IgE antibodies and Mast cells–May be genetic•Allergic rhinitis, allergies run in families •Familial but not a single gene characteristic. No tissue damage
Type 1
What 3 things make up the type 1 hypersensitivity?
Antigen
IgE antibodies
Mast cells
What are the primary mediators of mast cells?
Histamine
Proteases
Chemotactic factors
What are the secondary mediators of mast cells?
Prostaglandins
Leukotrienes
During the _____ encounter to an allergen:
•IgE antibody is induced by allergen
•Mast cells have high affinity receptors for the Fc end of IgE
•IgE binds via its Fc receptor to mast cells
FIRST ENCOUNTER
During the _____ encounter to an allergen:
•Antigen cross-links the fixed IgE
•Mast cell degranulation
•Pharmacologic effects of histamine, leukotrienes
SECOND ENCOUNTER
HOw does histamine affect bp, vasodilation, and permeability?
Decreases bp
Increases vasodilation
Increases permeability which lead to edema
During the _____ exposure to penicillin:
–PCN dose bridges Fab ends of two adjacent molecules •sends signal into mast cell cytoplasm to degranulate–Bronchioles constrict•Histamine, prostaglandins and leukotrienes cause smooth muscle contraction–If recognize in time –shot of epi –relax smooth muscle in bronchioles and vasoconstriction
Second exposure
During the _____ exposure to penicillin: –no reaction–May trigger an immune response by stimulating the Th2 pathway–Cytokines IL-4 (IgE molecules), IL-5 (recruits eosinophils)–Lots of IgE antibodies and eosinophils–IgE AB circulate have a high affinity for Mast cells in the skin and mucosa (Fc end of IgG)
FIRST EXPOSURE
Is anaphylactic shock a systemic or localized immediate hypersensitivity?
Systemic
Is angioedema a systemic or localized immediate hypersensitivity?
Localized
