Transcript LYMPHATICSYSTEMANDIMMUNITY
LYMPHATIC SYSTEM AND IMMUNITY CHAPTER 16
• HOW DOES IT TIE IN TO THE CARDIOVASCULAR SYSTEM?
• CIRCULATES BODY FLUIDS BACK TO THE BLOOD • WHAT WOULD HAPPEN IF IT DIDN’T
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LYMPHATIC PATHWAYS
• LYMPHATIC CAPILLARIES
LYMPHATIC CAPILLARIES
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LYMPHATIC CAPILLARIES
• HOW DO THEY DIFFER FROM BLOOD CAPILLARIES ?
• PARALLEL BLOOD CAPILLARIES • SIMILAR STRUCTURE • MORE FLUID EXITS CAPILLARIES ON ARTERIOLE SIDE THAN REABSORBED ON VENULE SIDE • INTERSTITIAL FLUID ENTERS= LYMPH • CELLS OVERLAP, AREN’T ATTACHED SO PROTIENS AND OTHER MATERIAL ENTERS WHEN PRESSURE INCREASES • FUNCTION OF LACTEALS ?
• GO TO LYMPHATIC VESSELS
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• HYDROSTATIC PRESSURE FORCES LYMPH IN • PROTEIN ATTACHMENT FIBERS
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• HOW DOES LYMPH FLOW THROUGH THE VESSELS?
– LIKE VEINS: • SKELETAL MUSCLE CONTRACTION • CONTRACTION OF RESPIRATORY MUSCLES • CONTRACTION OF SMOOTH MUSCLE IN LYMPH VESSELS • VALVES
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LYMPHATIC CAPILLARIES
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LYMPHATIC VESSELS
• STRUCTURE SIMILAR TO VEINS/ THINNER • SAME 3 LAYERS
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• SEMILUNAR VALVES
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LYMPHATIC TRUNKS
• LYMPHATIC VESSELS DRAIN INTO LYMPHATIC TRUNKS • NAMED FOR REGIONS THEY DRAIN • JOIN THE COLLECTING TRUNKS: • THORACIC DUCT – LARGER AND LONGER – FROM ABDOMINAL REGION TO LEFT SUBCLAVIAN VEIN – DRAINS INTESTINAL, LUMBAR, INTERCOSTAL TRUNKS, LEFT SUBCLAVIAN, LEFT JUGULAR, & LEFT BRONCHOMEDIASTINAL TRUNKS • RIGHT LYMPHATIC DUCT – RIGHT THORAX TO RIGHT SUBCLAVIAN VEIN • TO PLASMA
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LYMPH FLOW
• FLUID MOVEMENT FROM CAPILLARIES TO INTERSTITIAL FLUID TO LYMPH IS USUALLY BALANCED • OBSTRUCTION OF FLOW LEADS TO
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– EDEMA
LYMPH NODES
• USUALLY AFTER LYMPH VESSELS • ~1IN; BEAN SHAPED; HILUM; CAPSULE FORMS; LYMPH NODULES/FOLLICLES • AFFERENT LYMPH VESSELS ENTER AT VARIOUS AREAS ALONG CAPSULE • EFFERENT VESSLES EXIT AT HILUM
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LYMPH NODULES
• CONTAIN B LYMPHOCYTES AND MACROPHAGES TO FIGHT INVADING PATHOGENS WHY IN LYMPH NODES?
• SOME LYMPH NODULES ARE ASSOCIATED WITH OTHER SYSTEMS: – TONSILS – PEYER’S PATCHES: M CELLS (MICROFOLD) PICK UP ATIGENS FROM LUMEN OF SMALL INTESTINE AND BY TANSCYTOSIS 9VESSICLE MEDIATED) TRANSFER IT TO OTHER DENDRITIC CELLS AND T LYMPHOCYTES • LYMPH SINUSES PROVIDE PATHWAY FOR LYMPH TO CIRCULATE
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LYMPH NODE
en.wikipedia.org
Structure of the lymph node.
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Afferent lymphatic vessel
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6.
Sinus
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Nodule
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Capsule Valve to prevent backflow
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Medulla Efferent lymphatic vessel.
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LOCATIONS OF LYMPH NODES
• CERVICAL • AXILLARY • SUPRATROCHLEAR: MEDIAL SIDE OF ELBOW • INGUINAL • PELVIC • ABDOMINAL • THORACIC
LYMPH NODE FUNCTION
• FILTERING HARMFUL MATERIAL • IMMUNE SURVEILLANCE: LYMPHOCYTES AND MACROPHAGES
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THYMUS
• BILOBED; CAPSULE; MEDIASTINUM; ANTERIOR TO AORTIC ARCH; POSTERIOR TO STERNUM;TO PERICARDIUM • SHRINKS WITH AGE; ADIPOSE AND CONNECTIVE TISSUE FILLS IN • CONNECTIVE TISSUE FROM CAPSULE FORMS LOBULES • LOBULES CONTAIN LYMPHOCYTES (MARROW) MATURE INTO T LYMPHOCYTES DUE TO HORMONES THYMOSINS SECRETED BY EPITHELIAL CELLS OF THYMUS
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SPLEEN
• LARGEST LYMPHATIC ORGAN • UPPER LEFT ABDOMEN; INFERIOR TO DIAPHRAGM; ANTERIOR TO STOMACH • STRUCTURE SIMILAR TO LYMPH NODES; HILUM FOR BLOOD VESSELS AND NERVES; • VENOUS SINUSES FILLED WITH BLOOD
PULP
• WHITE PULP – TINY ISLANDS; SPLENIC NODULES PACKED WITH LYMPHOCYTES • RED PULP – REST OF LOBULES; SURROUND VENOUS SINUSES; CONTAINS RBCs, LYMPHOCYTES AND MACROPHAGES • CAPILLARIES OF RED PULP PERMEABLE: ALLOW RBCs TO PASS AND DAMAGED RBCs RUPTURE AND MACROPHAGES REMOVE DEBRIES • MACROPHAGES DESTROY PATHOGENS • LYMPHOCYTES DEFEND AGAINST INFECTIONS • SPLEEN FILTERS BLOOD
SPLEEN
SPLEEN
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SPLEEN
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SPLEEN
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BODY DEFENSES
• PATHOGENS: – BACTERIA; PROTOZOA; FUNGI; – VIRUSES • INFECTION DOESN’T ALWAYS HAVE SYMPTOMS • INNATE/NONSPECIFIC DEFENSES • ADAPTIVE/ SPECIFIC DEFENSES
INNATE DEFENSES
• SPECIES RESISTANCE • MECHANCIAL BARRIERS • CHEMICAL BARRIERS • NATURAL KILLER CELLS • INFLAMMATION • PHAGOCYTOSIS • FEVER
SPECIES RESISTANCE
• A SPECIES CAN’T GET CERTAIN DISEASES
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– DON’T HAVE THE RECEPTORS; OR DON’T HAVE CORRECT TEMPERATURE OR CHEMICAL ENVIRONMENT;
FIRST LINE OF DEFENSE MECHANICAL BARRIERS
• SKIN – SLOUGHS OFF REMOVING BACTERIA • MUCOUS MEMBRANES – CILLIATED EPITHELIUM • HAIRS TRAP INFECTIOUS AGENTS • SWEAT, MUCUS, TEARS, SALIVA, AND URINE WASH AWAY PATHOGENS
SECOND LINE OF DEFENSE
• CHEMICAL BARRIERS • ENZYMESGASTRIC – JUICE: PEPSIN & HCl – TEARS: LYSOSOMES – HCl – SALT – INTERFERRONS • HORMONELIKE PEPTIDES PRODUCED BY LYMPJHOCYTES OR FIBROBLASTS VS. VIRUSES AND TUMOR CELLS • HELP TO BLOCK THE REPRODUCTION OF VIRUSES • STIMULATE PHAGOCYTES AND OTHER CELLS TO RESIST INFECTION AND HINDER THE GROWTH OF TUMORS
• DEFENSINS – PEPTIDES MADE BY GRANULOCYTES OF INTESTINAL EPITHELIUM – GENES ACTIVATED BY SOME ANTIGENS OR VIRUSES FORM DEFENSINS – SOME MAKE HOLES IN CELL WALLS AND MEMBRANES • COLLECTINS – PROTEINS VS. BACTERIA, VIRUSES AND YEASTS – ATTACK THE DIFFERENT SUGARS ON PATHOGEN MEMBRANES MAKING IT MORE EASILY PHAGOCYTIZED
• COMPLEMENT SYSTEM: – GROUP OF PROTEINS IN FLUIDS REACT AS A CASCADE – BY ONE OF 2 PATHWAYS • CLASSICAL – ATTACHES TO ANTIBODY ATTACHED TO AN ANTIGEN • ALTERNATE – EXPOSURE TO ANTIGENS WITHOUT ANTIBODIES – STIMULATES INFLAMMATION ATTRACTS AND ENHANCES PHAGOCYTES
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NATURAL KILLER CELLS
• T LYMPHOCYTES • VS. CANCER CELLS AND VIRUSES • RELEASE PERFORINS
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INFLAMMATION
• • REDNESS, SWELLING, HEAT AND PAIN – HOW?
• DUE TO PATHOGENS (MAINLY); HEAT, UV, ACIDS, BASES • WHITE BLOOD CELLS INCREASE: – FIRST ?
– MONOCYTES BECOME MACROPHAGES – PUS ?
• EXUDATE: WITH CLOTTING FACTORS RELEASE FIBRIN FIBROBLASTS WALL OFF AREA TO INHIBIT SPREAD OF PATHOGENS/TOXINS
PHAGOCYTOSIS
• MOSTLY NEUTROPHILS AND MONOCYTES
DIFFERENCE?
• CHEMOTAXIS
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• MONOCYTES MACROPHAGES: FREE OR FIXED
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• MONONUCLEAR PHAGOCYTIC SYSTEM/RETICULOENDOTHELIAL SYSTEM
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FEVER
• BODY TEMP CONTROLLED BY ?
• SO WHAT CHANGES TO ALLOW FEVER ?
• VIRAL OR BACTERIAL INFECTION CAUSES LYMPHOCYTES TO RELEASE INTERLEUKIN 1/ ENDOGENOUS PYROGEN RAISES SET POINT • HIGHER TEMP CUASES LIVER AND SPLEEN TO HOLD IRON SO BACTERIA AND FUNGI CAN’T GROW • PHAGOCYTES ARE MORE ACTIVE ?
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ADAPTIVE DEFENSE (SPECIFIC)
• THIRD LINE OF DEFENSE: IMMUNITY – A RESISTANCE TO SPECIFIC PATHOGENS OR TOXINS AND OTHER BY-PRODUCTS • MUST DETERMINE SELF AND NON SELF ANTIGENS
ANTIGENS
• PROTEINS, POLYSACCHARIDES, GLYCOPROTIENS, OR GLYCOLIPIDS • BEFORE BIRTH SELF ANTIGENS ARE RECOGNIZED • LARGE AND COMPLEX CAUSE MORE RESPONSE • HAPTENS – SMALL MOLECULE THAT MAY CAUSE A RESPONSE WHEN COMBINED WITH A LARGER COMPOUND • DRUGS, DUST, DANDER, CHEMICALS
LYMPHOCYTE PRODUCTION
• DURING FETAL DEVELOPMENT UNSPECIALIZED LYMPHOCYTES RELEASED TO BLOOD • HALF GO TO THYMUS AND THYMOSINS MATURE THE T LYMPHOCYTES • MOST OF LYMPHOCYTES IN BLOOD • REST MATURE IN MARROW B LYMPHOCYTES • BOTH FOUND IN LYMPH NODES, SPLEEN, INTESTINAL LINING • BOTH ARE CLONED FROM ORIGINAL VARIETY CELL; EACH ONE HAS A ANTIGEN RECEPTOR SO ONLY RESPONDS TO A SPECIFIC ANTIGEN • B CELLS PRODUCE ANTIBODIES; T CELLS INTERACT DIRECTLY
T CELL RESPONSE
• ACTIVATED BY ANTIGEN-PRESENTING CELL LIKE SOME MACROPHAGES AND B CELLS • PHAGOCYTE DIGESTS BACTERIA ?
, SOME OF ANTIGEN TRAVELS OUT TO MAJOR HISTOCAMPATABILITY COMPLEX (MHC) (HUMAN LEUKOCYTE ANTIGENS/HLA) • FOUND ON ALL CELL MEMBRANES BUT RBCs (CLASS I) OR ON SURFACE OF ANTIGEN-PRESENTING CELLS, THYMUS CELLS AND ACTIVATED T CELLS (CLASS II)
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• MHC ANTIGENS HELP T CELLS RECOGNIZE FOREIGN ANTIGENS • CELLULAR IMMUNE RESPONSE: – ACTIVATED T CELLS REACT DIRECTLY WITH ANTIGEN PRESENTING CELL • T CELLS ALSO SECRETE POLYPEPTIDES: CYTOKINES: – INTERLEUKIN 1: ACTIVATES T CELLS; STIMULATES THEM TO RELEASE CYTOKINES – INTERLEUKIN 2: T CELL PROLIFERATION; STIMULATES T CELLS TO RELEASE CYTOKINES – CFSs STIMULATE BONE MARROW TO PRODUCE LYMPHOCYTES; CAUSE B CELLS TO GROW AND MATURE; ACTIVATE MACROPHAGES – INTERFERONS – TUMOR NECROSIS FACTOR: STOPS TUMOR GROWTH, CAUSES FEVER; STIMULATES LYMPHOCYTE DIFFERENTIATION; RELEASES GROWTH FACTORS – ALSO RELEASE TOXINS TO KILL ANTIGEN BEARING CELLS, AND GROWTH INHIBITING FACTORS
HELPER T CELLS
• ONCE ACTIVATED, STIMULATES B CELL TO PRODUCE ANTIBODIES VS. THE SPECIFIC ANTIGEN
CYTOTOXIC T CELL
• RECOGNIZES ANTIGENS OF CANCEROUS CELLS OR VIRALLY INFECTED CELLS • ACTIVATED BY CYTOKINES FROM HELPER T CELL • THEY CLONE: PROLIFERATE • BIND TO ANTIGEN BEARING CELL AND RELEASE PERFORIN
MEMORY T CELLS
• FROM CD8 T CELLS (CYTOTOXIC) • FOR FUTURE PROTECTION • CD8 T CELL CONTAQCTS ANTIGEN BEARING CELL IT FORMS A DUMBELL SHAPE – DIVIDES: ONE CELL BECOMES ACTIVE CYTOTOXIC CELL OTHER SIDE BECOMES A MEMORY T CELL • DURING SECOND INFECTION THIS CELL DIVIDES INTO CYTOTOXIC CELLS
B CELLS HUMONAL RESPONSE
• USUALLY ACTIVATED BY HELPER T CELL BUT SOME ARE DIRECTLY ACTIVATED (ANTIGEN) • WHEN B CELL ATTACHES TO ANTIGEN HELPER T CELL RELEASES CYTOKINES – STIMULATE PROLIFERATION OF B CELL – ATTRACT MACROPHAGES AND LEUKOCYTES • SOME OF THE B CELLS BECOME MEMORY CELLS
• SOME BECOME PLASMA CELLS – PRODUCE ANTIBODIES/ IMMUNOGLOBULINS – HAVE A LOT OF GA – 2,000 ANTIBODIES/MINUTE – CAN ONLY PRODUCE ONE TYPE OF ANTIBODY – POLYCLONAL RESPONSE: MORE THAN ONE ANTIGEN ?
• T CELLS CAN RELEASE CYTOKINES TO INHIBIT B CELL FUNCTION
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http://www.biokemi.org/assets/302/symphogen_02bg.jpg
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ANTIBODIES
• GAMMA GLOBULINS • SOLUBLE, GLOBULAR PROTIENS • 4 AMINO ACID CHAINS- DISULFIDE BONDS • 2 IDENTICAL LIGHT CHAINS AND 2 IDENTICAL HEAVY CHAINS • 5 DIFFERENT HEAVY CHAINS= 5 DIFFERENT ANTIBODIES • SPECIFIC SHAPE GIVES PHYSIOLOGY • VARIABLE REGIONS FIT ANTIGEN
• ANTIGEN BINDING SITE FORMS AROUND ANTIGEN AND IDIOTYPES IS PART THAT BINDS • REST IS CONSTANT REGION: BINDS TO CELL SRUCTURES OR CHEMICALS
IMMUNOGLOBULINS
• IgG: – 80%; PLASMA AND TISSUE FLUID; VS. BACTERIA, VIRUSES AND TOXINS; ACTIVATES COMPLEMENT; ANTI-Rh • IgA: – 13%; EXOCRINE SECRETIONS: BREAST MILK, TEARS, NASAL FLUID, GASTRIC JUICE, INTESTINAL JUICE, BILE, URINE; VS. BACTERIA AND VIRUSES
• IgM: – 6%; IN PLASMA; VS. FOOD, BACTERIA; ACTIVATES COMPLEMENT; ANTI-A/ANTI B; • IgD: – <1%; ON SURFACES OF MOST B CELLS, ESPECIALLY INFANTS; ANTIGEN RECEPTOR WHICH ACTIVATES B CELLS; • IgE: – <1%; EXOCRINE SECRETIONS LIKE IgA; PROMOTES INFLAMMATION AND ALLERGIC REACTIONS;
ANTIBODY ACTIONS
• DIRECT ATTACK • ACTIVATE COMPLEMENT • INFLAMMATION: LOCALIZED CHANGE
DIRECT ATTACK
• ANTIBODIES ANTIGEN = AGGLUTINATION OR PRECIPITATION – PHAGOCYTES GET THEM EASIER – NEUTRALIZE TOXIC PART
COMPLEMENT ACTIVATION
• IgG OR IgM + ANTIGENS EXPOSED REACTIVE SITES ON CONSTANT REGION = ACTIVATION OF COMPLEMENT PROTEINS WHICH CAUSE: – OPSONIZATION: COATING ANTIGEN ANTIBODY COMPLEX – MORE EASILY PHAGOCYTIZED – CHEMOTAXIS – CLUMPING – LYSIS OF MEMBRANES
INFLAMMATION
• IgE USUALLY ATTACHED TO MAST CELLS • ANTIGENS BIND AND STIMULATE MAST CELL TO RELEASE HISTAMINE • VASODILATION AND EDEMA
http://faculty.irsc.edu/FACULTY/TFischer/images/complement.jpg
IMMUNE RESPONSE
• PRIMARY RESPONSE – PLASMA CELLS RELEASES IgM, THEN IgG – TAKES HOURS TO DAYS, LASTS WEEKS – BUT: GET DISEASE – FORM MEMORY CELLS • SECONDARY RESPONSE – MEMORY CELLS ACTIVATED, PRODUCE IgG – FOLLICULAR DENDRITIC CELLS STIMULATE MEMORY CELLS
TYPES OF IMMUNITY
• ACTIVE VS. PASSIVE • NATURALLY ACQUIRED ACTIVE IMMUNITY – DISEASE • ARTIFICIALLY ACQUIRED ACTIVE IMMUNITY – VACCINE; SUBUNIT VACCINE – HERD IMMUNITY • ARTIFICIALLY ACQUIRED PASSIVE IMMUNITY – ANTISERUM; ANTITOXIN • NATURALLY ACQUIRED PASSIVE IMMUNITY – IgG THROUGH BLOOD; NURSING
ALLERGIES
• ALLERGEN • TYPES – IMMEDIATE REACTION/ANAPHALACTIC: TYPE I • INHERITED: OVERPRODUCE IgE; • PRIMARY RESPONSE ACTIVATES B CELLS • SECONDARY: QUICK RELEASE OF HISTAMINE, PROSTAGLANDIN D, LEUKOTRIENES • SEVERE INFLAMMATION • MAY NEED EPINEPHRINE OR DIE IN 5 MINUTES
• ANTIBODY-DEPENDENT CYTOTOXIC REACTIONS: TYPE II – TAKE 1-3 HOURS – SPECIFIC CELL BINDS ALLERGEN PHAGOCYTOSIS AND COMPLEMENT MEDIATED LYSIS – WRONG BLOOD TRANSFUSION • IMMUNE COMPLEX REACTIONS: TYPE III – TAKES 1-3 HOURS – PHAGOCYTOSIS AND COMPLEMENT CAN’T CLEAR ANTIGEN-ANTIBODY COMPLEXES – MAY BLOCK SMALL VESSELS AND CAUSE DAMAGE – AUTOIMMUNITY
• DELAYED-REACTION ALLERGY: TYPE IV – COULD AFFECT ANYONE – REPEATED EXPOSURE TO CHEMICALS – EVENTUALLY STIMULATES T CELLS – T CELLS AND PHAGOCYTES RELEASE CHEMICALS THAT CAUSE DERMATITIS – USUALLY TAKES 48 HOURS
TISSUE REJECTION
• MAY RECOGNIZE ANTIGENS AS FOREIGN – THE MORE DIFFERENT THE ANTIGENS ARE: MORE SEVERE RESPONSE – ANTIGEN MATCH – TYPES OF TRANSPLANT TISSUE • ISOGRAFT: IDENTICAL TWIN • AUTOGRAFT: SAME PERSON • ALLOGRAFT: ANOTHER PERSON • XENOGRAFT: DIFFERENT SPECIES • GRAFT-VERSUS-HOST DISEASE: TISSUE MAY PRODUCE CHEMICALS THAT HARM RECIPIENT • MAY USE IMMUNOSUPRESSIVE DRUGS PROB ?
(BEFORE)
AUTOIMMUNITY
• CAN’T TELL SELF VS. NONSELF • AUTOANTIBODIES AND CYTOTOXIC T CELLS ATTACK BODY’S TISSUES • CAUSES: NOT SURE – VIRUS COAT WITH HUMAN PROTEIN – T CELLS DON’T LEARN SELF ANTIGENS IN THYMUS – NONSELF TOO CLOSE TO A SELF – FETAL CELLS CIRCULATING IN WOMAN TRIGGERED SOMEHOW TO STIMULATE ANTIBODIES: MICROCHIMERISM – SCLERODERMA
LIFE SPAN CHANGES
• THYMUS SHRINKS • 70: IMMUNE SYSTEM AT 25% • MORE SUSCEPTIBLE TO CANCER AND DISEASES LIKE INFLUENZA • T CELL NUMBER DECREASES SLIGHTLY, B CELL DOESN’T • ANTIBODY RESPONSE SLOWS: VACCINES ?
• IgA, IgG INCREASE %; IgD, IgE DECREASE; MORE AUTOANTIBODIES • HAVE TO BE CAREFUL WITH IMMUNOSUPRESSIVE TREATMENTS