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?
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
en.wikipedia.org
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
en.wikipedia.org/
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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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:
– <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 ANTIGENANTIBODY 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