Hallmark of type 3 HR

Period of sensitization in type 1 HR

Complement bind to immunoglobulin structure

In rheumatoid arthritis, antibodies deposited on the organs involved

Autoimmune disorder type 2 hypersensitivty plays significant role

Symptom of anaphylaxis, severe type of hypersensitivity reaction

Vasodilation Type 1 hyper caused by whuch molecule

Anaphylactic shock Bee sting reaction Which cell type

Complement proteins are

Stabilizes binding C3 convertase of alternative pathway

Mhc class present antigens cytotoxic T cells

Adaptive humoral mediated immunity

Secondary immune response

Transplacental transfer of antibodies

Type 4 hypersensitivity reaction

Dry mucous membrane and changes in taste 3 weeks after an unidentified viral illness

Regulatory T cell - Regulate function of immune cells Recognize self from non self - immune tolerance

destroy antigen via perforin granzyme Activation of APOPTOSIS

Re encounter with similar antigen promoting antibody synthesis except IgM

initiate inflammation IgM, IgG synthesis Delayed hypersensitivity

.

Limited ability to cause disease Protection against enveloped viruses mimic natural infection Immunity acquired long lived

Exotoxins Require multiple doses Not as immunogenic

Transplant and graft rejection

CD8 + t cells

Phagocytosis Natural killer cells

Antigen destroyed by specific cells

Most abundant in serum Monomer Only immunoglobulin capable of crossing the placenta

Surface marker for B cells

Innate humoral immunity

Peripheral lymphoid organ

Central lymphoid organ

Site of differentiation and maturation of immune cells

Site where T cells and B dells encounter antigens for destruction

Cd4+cd25+t cells

Large granular lymphocytes

Helper T lymphocytes

Cytotoxic T lymphocytes

Adaptive cell mediated Destroy antigens Defense against intracellular organisms and tumor cells

B cells Macrophages Dendritic cells

Glial (cns) Kupffer (liver) Langerhan (skin) denditric

Local and systemic anaphylaxis

Triggers: peanuts, seafood, bee venom, aspirin, penicillin

specific patterns of sugars (bacterial cell wall) C1 and C3 → C4b2a

Antigen antibody complexes C1qrs (recognition unit) Cleavage of complement proteins C2 and C4 → c4b2b Both innate and adaptive

Propedin pathway Activated by bacterial products (endotoxin/complexes of immunoglobulins) innate immunity

Intracellular pathogens (Mycobicterlum tuberculosis) viruses and fungi delayed type

Either inflammation brought about by cytokines produced by

Direct killing of target cells

T lymphocytes not antibodies

Delayed type

Local immune - Arthus reaction systemic immune - acute serum sickness, splenomegaly, lymphadenopathy, urticaria, joint pain

Kidneys and blood vessels endothelium fibrinoid necrosis Kidneys in Malaria (black water fever) Dengue Hepatitis B ( polyarteritis nodosa)

Immune complex mediated hypersensitivity

Cytotoxic or cytolytic

3rd subtype: antibodies directed against specific cellular receptors Myasthenia gravis Grave's disease Hyperthyroidism

2nd subtype: complement and Fc receptor mediated inflammation

1st subtype: opsonization and phagocytosis

Severe allergy response: hypotension, severe bronchoconstriction, laryngeal edema

Food allergy Urticaria (hives) Eczema allergic rhinitis hay fever asthma

Cellular events Infiltration by inflammatory cells Neutrophils and eosinophils LEukotrienes

Vascular events of inflammation vasodilation Increase vascular permeability histamine Reaction within minutes of re-exposure

Immediate (anaphylactic) hypersensitivity

CD8+ Main defense against intracellular organisms such as viruses And tumor cells

Stimulate differentiation of B cells to antibody producing plasm cella ACTIVATE CYTOTOXIC T CELLS

Recruit neutrophil lead to inflammation

Re-exposure to same antigen Stimulating class switching to form antibodies

First exposure Stimulate inflammation Delayed HR IgG and IgM

involves both helper and cytotoxic t cells

Defense against extracellular and encapsulated organism, toxin producing microbes Neutralize viruses

Surface marker for B cells No biologic activity

reaginic antibody Predominant in type 1 hypersensitivity and parasitic infections

Secretory immunoglobulin Prevent adhesion to mucosal surface Protection to GIT, digestive tract, genitourinary tract

Acute inflammation Primary immune response Largest More effective fixer of complement Antigen receptor on the surface of B cell

Major immunoglobulin Secondary immune response Function as opsonin Cross the placenta Chronic inflammation fix complement

Synthesis of specific antibodies by activated B cell

Natural killer cells Phagocytic cells

Specific proteins Destroy antigens Cytokines and complement

T cell Either CD4+T cell (delayed) CD8+ T cell (cytotoxic t cell mediated)

Acute serum sickness - systemic form Arthus reaction - localized form

Immune complex IgG and IgM Fibrinoid necrosis

Antibody Antigen-antibody complexes Activation of the classical pathway of complement system IgG and IgM