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?

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 ? • 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 ? • 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 ? – 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

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Structure of the lymph node. 1. Afferent lymphatic vessel 2. Sinus 3. Nodule 4. Capsule 5. Medulla 6. Valve to prevent backflow 7. 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 ? – 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 ?

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 ? • MONOCYTES  MACROPHAGES: FREE OR FIXED ? • 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 NONSELF 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/ANTIB;

• IgD: –