Lymphatic System Flashcards
Lymphocytes
Lymphatic system cells respond to:
1) environmental pathogens
2)toxins
3) abnormal body cells (ex. Cancer)
Lymphocyte circulation
-from blood➡️IF (lymph) through capillaries
-returns to venous blood through lymphatic vessels
-also transports hormones, nutrients, and waste products
Lymphatic vessels
-carry lymph
-lymphatic system begins w/ smaller vessels
-lymphatic capillaries (terminal lymphatics)
Thoracic duct
-collects lymph from (3/4 of the body):
-left bronchiomediastinal trunk
-left subclavian trunk
-left jugular trunk
-empties into left subclavian vein
Base of thoracic duct
■ Expands into cisterna chyli
■ Cisterna chyli receives lymph from:
■ right and left lumbar trunks
■ intestinal trunk (spleen, stomach, intestine, pancreas, lower front liver)
Cytotoxic T cells
Effector CD8
■ Attack cells infected by cancer or viruses
■ Produce cell-mediated immunity
Helper T cells
Effector CD4- humoral and cellular immunity
■ Stimulate function of T cells and B cells
-➕production of T cells and plasma cells
-➕macrophages
-act directly and indirectly by releasing cytokines (small proteins that act as chemical messengers in the immune system, signaling cells to fight threats and regulate the immune response)
Suppressor T cells
■ Inhibit function of T cells and B cells
B cells
Lymphocyte that matures in bone marrow
■ Make up 10–15% of circulating lymphocytes
■ Differentiate into plasma cells and memory cells
-via progeny (clone members)
Plasma cells
Antibody (immunoglobulin proteins) producing machine
Effector B cell
Regulatory T cell
Effector CD4 T cells
Slows or stops activity of immune system
Important in controlling autoimmune diseases
NK cells
-responsible for immunological surveillance (non specific/“nonself”
-attack:
-foreign cells
-virus-infested cells
-cancer cells
Lymphoid nodule
-areolar tissue w/ densely packed lymphocytes
-germinal center contains dividing lymphocytes
Lymph nodes
Site of lymphocyte activation and proliferation
■ Act as filters for lymph fluid (cleanse lymph)
■ Embedded in connective tissue, in clusters along lymphatic vessels
■ Near body surface in inguinal, axillary, and cervical regions of body
Thymus
Site of T cell maturation
■ Located in mediastinum
■ Deteriorates after puberty:
■ diminishing effectiveness of immune system
Spleen functions
- Removal of abnormal blood cells and other blood components by phagocytosis
- Storage of iron recycled from red blood cells
- Initiation of immune responses by B cells and T cells:
■ in response to antigens in circulating blood - The Stores blood platelets and monocytes
- May be site of fetal erythrocyte production (normally ceases before birth)
Complement activation
-complements work together in cascades
-2 pathways activate complement system
-Classical
-alternative
Complement system
Works WITH antibodies to trigger inflammation
group of proteins that work together to help the body’s immune system fight infection and pathogens
Part of innate immune system
Classical pathway
■ Fast method
■ C1 binds to or is fixed to antibody molecule attached to antigen (bacterium)
■ Bound (fixed) protein acts as enzyme:
■ catalyzes reaction between other C proteins
4 effects of complement activation
- Stimulation of inflammation - stimulates histamine release
- Promoting chemotaxis - Attraction of phagocytes to areas of pathogens
- Opsonization
▪ Enhancement of phagocytosis by :
■ complements working with antibodies (opsonins) to coat pathogens and make it easier for macrophages to bind - Destruction of target cell:
■ 5 complement proteins join to form membrane attack complex (MAC)
4 effects of inflammation
- Temporary repair and barrier against infection
- Retards spread of pathogens into surrounding areas
- Mobilization of local and systemic defenses:
■ and facilitation of repairs (regeneration) - Alerts adaptive immune system
Inflammation
■ Begins with chemicals released into ECF by injured tissues, immune cells, blood proteins
■ Macrophages and epithelial cells of boundary tissues bear Toll-like receptors (TLRs)
■ 11 types of TLRs recognize specific classes of infecting microbes
■ Activated TLRs trigger release of cytokines that promote inflammation
Innate immunity
Genetically determined- no prior exposure of antibody production involved
-mast cells
-neutrophils
-monocytes
-dendritic cells
-macrophages
-NK cells
Aquired immunity (adaptive)
Produced by prior exporsure or antibody production
-B cells w/ antibodies
-T cells
-regulatory T cells
-dendritic cells
-macrophages
-NK cells
Active immunity
Produced by antibodies that develop in response to antigens (immune response)
Induced active immunity
Develops after administration of antigen to prevent disease
Naturally acquired active immunity
Develops after export antigens in environment
Passive immunity
Produced by transfer of antibodies from another person
Natural acquired passive immunity
Conferred by transfer of maternal antibodies across placenta or in breast milk
Induced passive immunity
Conferred by admin of antibodies to combat infection
Why is complement system considered innate immune system?
While antibodies are part of the adaptive immune system (acquired immunity), the complement system itself is a set of proteins that can be activated directly by pathogens without the need for specific antibody recognition, making it a key component of the innate immune response.
Specific defenses
When you are exposed to something from outside the body, and it activates T cells and B cells
Responds to specific antigens
With coordinated action of T cells and B cells
Antigen
An antigen is a substance that signals the immune system to determine if something in the body is harmful. Antigens can be found on bacteria, viruses, tumors, and even normal cells
Collection of antigenic determinants or epitopes (specific region of an antigen that the immune system recognizes)
-each epitope ➕ development of T cell and B cells
Antigen presenting cells
■ Responsible for activating T cells against foreign cells and proteins
■ Located in places where antigens are likely to enter the body
■ Can take in antigens by pino- or phagocytosis
■ After processing antigens - migrate to lymph nodes via lymph vessels
Dendritic cells, B cells, macrophages
Incomplete antigens/ haptens
Antigens that are unable to trigger an immune response on their own are called incomplete antigens or haptens
Must attach to a carrier molecule to act as a complete antigen
Hapten dangers
Autoimmune disease and allergy
Complete antigen
substance that can both trigger an immune response and react with the products of that response
■ Has 2 antigenic determinant sites
■ Binds to both of antigen binding sites of variable segments of antibody
MHC proteins
Membrane proteins that bind to antigens
■ The major histocompatibility complex (MHC) are nprotein molecules (self-antigens) on surface of cells not antigenic to self but antigenic to others in transfusions or grafts
■ Self identifiers
■ Genetically coded in chromosome 6:
■ differs among all individuals except identical twins
■ Also called HLA – Human Leukocyte Antigens
Classes of MHC proteins
■ Class I:
■ found in membranes of all nucleated cells
■ Reason for rejection of transplanted organs
■ Class II:
■ found in membranes of antigen-presenting cells (APCs)
■ Including macrophages, dendritic cells
■ Also found on B cells
MHC 1 protein
All cells
■ Pick up small peptides in cell and carry them to the surface
■ T cells ignore normal peptides
■ abnormal peptides or viral proteins activate T cells to destroy cell
(Hey, come kill me!)
MHC 2 proteins
Only on immune cells- antigen presenting cells
■ Antigenic fragments: (Present only in lymphs)
■ from antigenic processing of pathogens
■ bind to Class II proteins
■ inserted in cell membrane to stimulate naive T cells
(sick-em Boys)
CD markers
“Cluster differentiation makers”
-T cell membranes
-molecular mechanism of antigen recognition.
CD4
On cells that are going to become helper T cells or suppressor cells
CD8
On cells that become cytotoxic T cells
Activation of cytotoxic T cells
-require helper T cells
-bind directly to infected cells
■ Activated by exposure to antigens on MHC 1 proteins presented by infected cells or APCs (dendritic cells)
T cell activation
process in the immune system that occurs when a T cell binds to a foreign peptide or mutant peptide on a diseased cell
B cell activation
-recognize something in environment- recognizes
-require helper T cells
-naive B cell require antigen binding B cell
-(become plasma cells) make antibodies only after helper T cells comes in
-
4 allergy reaction types
■ Type I:
■ immediate hypersensitivity
■ Type II:
■ cytotoxic reactions
■ Type III:
■ immune complex disorders
■ Type IV:
■ delayed hypersensitivity
Functions of cytokines
- Stimulate T cell divisions:
■ produce memory T cells
■ accelerate cytotoxic T cell maturation - Attract and stimulate macrophages
- Attract and stimulate immune cells
- Promote activation of B cells
Antibody structure
Constant segment determines antibody type
Variable segments- binding site
IgM
■ Largest Ig in size (pentamers)
■ due to its size it is restricted to the blood and cannot cross membranes;
■ excellent Complement (C’) fixer; first to appear in the primary immune response.
■ Includes the blood type agglutinins.
■ Accounts for approximately 5-10% of circulating Ig.
■ Also exists as a monomer which serves as antigen receptor on B cells
Clump up blood vessels
IgG
■ Smaller Ig and therefore can leave the blood to cross membranes including those of the
■ Excellent C’ fixer - binds C’ aggressively.
■ First to appear in significant quantity in the secondary, anamnestic or booster response
■ includes the antitoxins, accounts for 75-80% of circulating Ig
IgA
■ Secretory Ig – Mostly a dimer
■ found in abundance in most bodily secretions including tears, saliva, semen, milk, colostrum, mucus.
■ Attack pathogens before they enter the body (by binding to them on mucosal surfaces- GI, respiratory)
■ Accounts for approximately 10-15% of circulating Ig.
■ Levels decrease during stress
IgD
■ Rare Þ 2,000 times less abundant in blood than IgG.
■ Acts as antigen receptor on B cells along with IgM.
■ Function not well understood
IgE
■ Found on mast cells and basophils
■ aka Atopic Ab, Skin Sensitizing Ig, Anaphylactic Ab, Allergic Ab, Reaginic Ab
■ Not found in large quantity in the blood because once formed it exits the blood to attach to mast cells in connective tissue
■ Stimulates release of histamine and other chemicals which regulate inflammation
■ It is responsible for all Type-I immediate hypersensitivity reactions including atopy and anaphylaxis.
Primary Respondes
IgM produced
■ Takes time to develop
■ Antigens activate B cells
■ Plasma cells differentiate
■ Antibody titer (level of Ab activity) slowly rises
■ Peak response:
■ can take 2 weeks to develop
■ declines rapidly
■ IgM:
■ is produced faster than IgG
■ is less effective
Secondary immune responses
IgG antibodies produced- fetal blood response
■ Activates memory B cells:
■ at lower antigen concentrations than original B cells
■ secrete more effective antibodies in higher qualities
Specific adaptive immunity
- second line of immunity
- can protection against same pathogen that is exposure in the last (has memory component)
- composed of highly specialized cells and process that eliminate or prevent pathogen growth
- response is antigen dependent
- lag time between exposure and maximal response
- antigen specific
- immunologic memory
Nonspecific or innate immunity
- first line of immunity against invading organisms
- present at birth
- called this name because its components treat all foreign substances in the same way
- response is antigen independent
- immediate maximal response
- antigen nonspecific
- no immunologic memory
Type 1 reaction
■ Also called immediate hypersensitivity
■ A rapid and severe response to the presence of an antigen
■ Most commonly recognized type of allergy
■ Includes allergic rhinitis (environmental allergies)
■ Affects 15% of the population
■ Sensitization leads to:
■ IL-4 secreted by TH cells stimulating B cells
■ production of large quantities of IgE antibodies
■ distributed throughout the body where they bind to the membranes of mast cells and basophils (Genetic component?)
■ Second exposure leads to:
■ stimulation of these IgE antibodies on the mast cells and basophils
■ massive inflammation of affected tissues
■ due to the release of histamine, prostaglandins and leukotrienes
■ Severity of reaction depends on:
■ individual sensitivity
■ locations involved
■ Allergens in blood stream may cause anaphylaxis
Type 2 reaction
■ Cytotoxic Reactions
■ Mediated by IgG, IgM and Complement (C’) which attack formed elements in the blood
■ Damage is often due to cytolysis and/or attraction of phagocytic cells which release lytic enzymes h
■ Manifestations include:
■ Erythroblastosis fetalis
■ blood transfusion incompatibility reactions
■ Thrombocytopenia
Type 3 reaction
■ Immune Complex Disorders
■ Mediated by IgG or IgM and sometimes complement (C’)
■ Damage is often due small immune complexes which become trapped in the basement membrane of blood vessels
■ cause serious inflammatory responses
■ Manifestations include:
■ Glomerulonephritis – inflammation of the glomeruli of the kidneys
■ Systemic Lupus Erythematosus (SLE) - a chronic, inflammatory autoimmune disorder affecting the joints, skin, kidneys and other organs (may also include some Type II characteristics),
■ Rheumatoid Arthritis
Type 4 reaction
■ Delayed type hypersensitivity- Mediated Immunity (CMI)
■ Occur 12-72 hr after exposure
■ Mediated by T lymphocytes including Cytotoxic T lymphs (TC) and Delayed Hypersensitivity T lymphs (TDh)
■ APCs migrate to lymph nodes and T cells go back to the point of exposure
■ Damage is due to lymphokines produced and secreted by T lymphs. Host mast cells may be destroyed, thus inducing inflammation.
■ Manifestations include:
■ Graft/Tissue rejection
■ Allergic Contact Dermatitides (ACDs)
■ Tuberculosis
