Ch. 21: Lymphatic and Immune Systems
I. Lymphatic System
An open system of vessels. Functions: fluid recovery; immunity; lipid absorption
and transport. Components: lymph; lymph vessels; lymphatic tissue; lymphatic
organs.
(A) Lymph and Lymphatic Vessels Lymph similar to plasma but with less
protein. Collected by lymph capillaries (extra leaky). Vessels similar to veins.
Capillaries -> collecting vessels -> lymphatic trunks -> collecting ducts = right
collecting duct and thoracic duct (on left), which is larger. Flow similar to
venous flow. Enhanced with surrounding muscle contraction, valves.
(B) Lymphatic Cells and Tissue
-1- T Cells
-2- B Cells
-3- Macrophages: display foreign antigens (Ags), one type of ‘antigen presenting
cell’ (APCs).
-4- Dendritic cells: APCs in skin (Langerhans), mucous
membranes and lymphatic organs.
-5- Reticular cells: branched,
help form stroma of lymphatic organs, act as APCs in thymus.
Diffuse lymphatic tissue throughout body, often called MALT (mucosa associated
lymphatic tissue). Also forms nodules (transient) and clusters (Peyers
patches).
(C) Lymphatic Organs
-1- lymph nodes: cleanse lymph and notify immune cells of pathogens. Many in
cervical, axillary, inguinal areas. Also in body cavities. Divided into
compartments by connective tissue. Contain lymphocytes and APCs. Afferent
and efferent lymphatic vessels. When swollen = lymphadenitis.
-2- tonsils: crypts lined with nodules.
b. palatine
c. lingual
a. pharyngeal = adenoids
-3- thymus: lymphatic and endocrine functions. T Cell development.
-4- spleen: red pulp with RBCs; white pulp with lymphocytes and macrophages.
Filters blood, removes aged RBCs. Vulnerable location.
II. Nonspecific Resistance
Defenses against pathogens: disease-causing organisms. External barriers,
antimicrobial mechanisms, immune system.
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(A) External Barriers: skin, mucous membranes, secretions: tears, sweat,
saliva, gastric…..
(B) Leukocytes and Macrophages – phagocytic
-1- leukocytes
a. neutrophils – combat bacteria with respiratory burst, uses lysosomes
to release toxins. Create killing zones.
b. eosinophils – phagocytize Ag/ Ab complexes, allergens, combat
parasitic worms.
c. basophils – release heparin and histamine to enhance action of other
WBCs.
d. lymphocytes – NK cells nonspecific, combat cancerous or infected
host cells. Immunological surveillance. Secrete perforins.
-2- macrophages
Include histiocytes in loose CT; dendritic cells in skin; microglia in
CNS; alveolar macrophages; hepatic macrophages.
(C) Antimicrobial Proteins
-1- interferons: inhibit viral reproduction.
-2- complement: at least 20 proteins, activated by pathogens. Results in
enhanced inflammation, opsonization: makes bacteria easier to phagocytize,
cytolysis.
(D) Inflammation – redness, swelling, heat and pain triggered by
chemicals such as histamine, leukotrienes. Three processes:
-1- mobilization of defenses: vasodilation, hyperemia. Leukocyte diapedesis.
-2- containment and destruction of pathogens. Chemotaxis attracts
neutrophils.
-3- tissue cleanup and repair. Monocytes transform into macrophages.
Edema, pus- collects in abscesses.
(E) Fever = pyrexia. Adjective: febrile. WBCs release pyrogens.
Promotes interferons, increases metabolism, inhibits microbial reproduction.
III. Specific Immunity Overview
Advantages = specificity and memory.
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(A) Forms of Immunity
-1- Cell mediated: direct attack of ‘suspicious’ cells. Results in lysis or
enhancement of non-specific defenses.
-2- humoral = antibody mediated.
a. natural active – sickness experience.
b. artificial active – vaccination
c. natural passive – via placenta, milk.
d. artificial passive – gamma globulin injections.
No memory with passive forms.
(B) Antigens Molecules which trigger immune responses.
(C) Lymphocytes T and B Cells
(D) Antigen Presenting Cells Present Ags on MHC (major
histocompatability complex) Proteins, which are genetically programmed.
(E) Interleukins – released by WBCs.
IV. Cellular Immunity
Involves Cytotoxic T Cells = Killer Ts; Helper Ts; Suppressor Ts; Memory Ts.
(A) Recognition
-1- antigen presentation: occurs in lymph nodes. Cytotoxic and Helper Ts
respond to APCs.
-2- T Cell Activation: costimulation (double check) results in clonal selection.
(B) Attack
-1- Helper Ts: attract neutrophils and NK Cells, macrophages. Stimulate T and B
Cell mitosis and maturation.
-2- Cytotoxic T Cells: directly attack and kill infected cells, transplants, cancer
cells.
-3- Suppressor Ts: inhibit T and B Cells as pathogen disappearing. Prevents
autoimmunity.
(C) Memory - Some Cytotoxic and Helper Ts become memory cells.
Create much faster response upon secondary exposure.
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V. Humoral Immunity
(A) Recognition – B Cells bring antigens in via receptor-mediated
endocytosis, then display some on MHC proteins. If Helper Ts bind, they
activate B Cells into clonal selection. Most are plasma cells, which produce
antibodies (2000/ sec).
(B) Attack – antibody (Ab) structure: four polypeptides, two heavy & two
light, each with variable (forms AG bindings sites) and constant regions.
-1- Five Ab Classes
a. IgA in secretions- blood, mucous, saliva, tears, milk…..
b. IgD on B Cell membranes
c. IgE in tonsils, skin, mucous membranes.
d. IgG are most circulating Abs, cross placenta.
e. IgM on B Cell membranes.
Can be customized via different combinations of ~35,000 genes.
-2- mechanisms
a. neutralization: AB binds to pathogenic portion of Ag.
b. complement fixation: IgM and IgG expose foreign cells to complement
.
c. agglutination: prevents spread of pathogens.
d. precipitation: follows agglutination.
(C) Memory – Memory B Cells responsible for much faster secondary
response.
VI. Immune Disorders
(A) Hypersenitivity – allergies = responses to allergens. Most common is
Type I (acute). May lead to anaphylaxis.
(B) Autoimmunity – failures of self-tolerance. Rheumatoid arthritis; Type I
DM; lupus; MS,….
(C) Immunodeficiency SCID; AIDS – infects Helper Ts, dendritic Cells
and macrophages. Problem = opportunistic infections.
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