friday intro to immune system fun video! monday: work on immune stuff with sub. thursday:...

32
Friday Intro to immune system Fun video! Monday: Work on immune stuff with sub. Thursday: Test…nervous and immune

Upload: frederick-oliver

Post on 03-Jan-2016

216 views

Category:

Documents


2 download

TRANSCRIPT

Friday

Intro to immune system Fun video! Monday: Work on immune stuff with

sub. Thursday: Test…nervous and immune

Immunity In a Nutshell

Figure 43.4 The human lymphatic system

Figure 43.1 An overview of the body's defenses

Part One: Non Specific Immunity

First Line of defense Skin: physical barrier, oily & acidic Mucus membrane: Lining of mouth, and

lungs (ciliated) Secretions of mucus membrane: tears,

sweat, contain lysozymes.

Part One: Non Specific Immunity

Second Line of defense Phagocytosis: attack, ingest, destroy

– Neutrophils: majority of WBC, chemotaxis– Macropahge: (monocyes) very large– Eosinophils: attack parasites and foreign

compounds coated with antibodies– Natural Killer: destroy infected/cancerous

cells (surveillance)

Part One: Non Specific Immunity

Second Line of defense Antimicrobial Proteins

– Complement system: the “usher”, assist in bringing pathogen to phagocyte

– Interferon: distress signal proteins secreted from virus infected cells

Part One: Non Specific Immunity

Second Line of defense

Part One: Non Specific Immunity

Second Line of defense Inflamatory Response: when skin breaks

– 1. Histamine: secreted by basophils and mast cells causes vasodilatation

– 2. Vasodilatation increases blood supply to injury. Causes redness, heat and swelling

– 3. Phagocytosis: macrophages and neutrophils arrive to injest and destroy pathogens

– 4. Pyrogens and pus: pus is an accumulations of dead WBC. Pyrogens increase body temp.

Part Two: Specific Immunity

Specific immunity terms…..

Active Immunity = Immunity conferred by an encounter with the actual virus or bacterium. The body produces antibodies in its own defense.

Passive Immunity = Temporary acquired antibodies passed on to the organism. No antigen is passed on. Mother’s breast milk to infant.

More terms….

Immune Response: a recognition system that distinguishes "self" form "non-self".

Antigens: any foreign material (proteins or saccharides) that elicits an immune response

Antigen presenting cell (APC) = infected body cell that is “presenting” a piece of an antigen (ex. Bacteria) on in cell surface to alert lymphocytes for more assistance.

Last but not least….

MHC: (major histocompatability complex)– Group of glycoproteins that tell the difference

between “self” and “non-self”. – Located on ALL cells, they are antigens

presenters. – Antigen presenting cell (APC) displays portion of

antigen on the surface of the cell using an MHC

ANTIGEN PRESENTINGMacrophage

Lysozome has eaten bacteria..Yummy!

Old bacteria bits

MHC is “presenting

” antigen

Nucleus

T-cells

Originate in bone marrow, mature in thymus

Receptors on T-cells are specific (complementary) to MHC’s

Macrophage ingestion of antigen and MHC presentation

Figure 43.9 The interaction of T cells with MHC molecules

Antigen presenting cell and T-cell saying “hello”

Daughter T cells

Cytotoxic T-cells: destroy “non-self” cell by secreting perforin which ruptures the antigens infected cell

B cells

Originate and mature in bone marrow (“B” for bone)

Membrane surface contain antibodies

Properties of antibodies

Proteins, may be free floating or bound to B-cells

Each is specific to an antigen

5 classes of immunoglobulins (Ig’s) IgA, D, E, G, M

Figure 43.6 Clonal selection

Autoimmune diseases

Vitiligo

a pigmentation disorder in which melanocytes (the cells that make pigment) in the skin are destroyed.

Patients with Vitiligo develop white spots in the skin that vary in size and location.

The disease affects both sexes and all races however; the distinctive patches are most noticeable in people with darker skin tones

QuickTime™ and aTIFF (Uncompressed) decompressorare needed to see this picture.

QuickTime™ and aTIFF (Uncompressed) decompressor

are needed to see this picture.

Butterfly rash of lupusDamaged kidney (left) caused by immunoglobulin deposits (right)

Systemic Lupus Erythematosus a chronic systemic autoimmune disease

– Complexes of anti-self antibodies and antigen deposit in, and cause damage to, tissue

1 million sufferers in the U.S.– Strikes women nine times more often than men

symptoms may include butterfly-shaped rash on face, fatigue, headaches triggered by environmental effects in persons who are genetically susceptible

Rheumatoid Arthritis (RA) chronic systemic autoimmune disease

- anti-self antibodies that react with the constant regions of other antibodies (rheumatoid factor)

onset of disease occurs most often between the ages of 25-55– women are 3 times more likely to develop this than men

symptoms include weakness, fatigue, and joint pain infections, hormones and genetic factors may be

involved

X-ray shows severe arthritis affecting the joints and limiting mobility

Figure 43.x3 X-ray of hands with arthritis

Multiple Sclerosis (MS) chronic organ-specific disease - may be mild or severe

– involves the destruction of the myelin sheath that covers cells of the spinal cord and brain

affects ~ 1 in 1600 people– 60% of the cases occur in women

symptoms include weakness, tremors or paralysis of one or more extremities, numbness, decreased memory and attention span and may disappear and recur over time

infections, hormones and genetic factors may be involved

Magnetic resonance image of brain of patient with chronic form of multiple sclerosis, showing characteristic lesions of MS (white spots)

Juvenile Diabetes also known as Type I diabetes or insulin-dependent

– beta-cells in the pancreas produce little or no insulin. usually occurs before the age of 30

– occurs in 1 in 7000 children each year– incidence decreases after the age of 20

symptoms include increased thirst and urination, weight loss, nausea, fatigue

cause is linked to genetic, viral, and autoimmune factors

Normal pancreas

Diabetic pancreas

Treatments for autoimmune diseases

current treatments are based on easing disease symptoms– anti-inflammatory drugs to reduce the inflammatory response– cytotoxic drugs to kill immune cells– treatments that block interaction of immune cells – e.g., bind to

cytokines, block second signals– replacement of necessary chemical – e.g., injections of insulin for

diabetes– changes in diet– exercise

in the future– gene therapy– vaccines to turn off the autoimmune response

Under-reaction to antigen

occur when some part of the immune system is defective or missing– T cells, B cells, phagocytes, or complement

these deficiencies are grouped as:– primary: inherited or congenital

• severe combined immunodeficiency

(SCID)– secondary: acquired

• HIV infection

David Vetter 1972-1984, the original bubble boy

Immunodeficiencies