Blood and antibodies

Campbell and Reece
Chapter 43 - immune system
also look back at chap 42 for blood

I. Plasma - (serum lacks fibrinogen) fluids, nutrients, O2, CO2, ions
proteins (synthesized in liver except gamma globulins)(clotting)

II. Hematocrit TRANSPARENCY (Fig. 42.14)
Erythrocytes 5-6 million/ml
Leucocytes 5-10 thousand/ml
Platelets 250,000-400,000/ml from megacaryocytes
(antibodies) ions, wastes, hormones

Platelets 250,000/ml from megacaryocytes
Clotting Platelet adhesion then fibrin (from fibrinogen) TRANSPARENCY (Fig. 42.16)
activated Hageman factor
prothrombin -> thrombin
fibrinogen ->fibrin
Hemophelia is famous disorder covered in Bio 104 genetic disease lecture.

Cells -

Red blood cells (corpuscles) (erythrocytes)
no nuclei
O2 transport, hemoglobin, anemia
last 120 days, made in marrow, recycled
iron recycling in liver is what makes feces dark (and skin yellow in jaundice [hepatitis]) - bile pigments

There are non-specific responses to injury

White blood cells (leucocytes as in leukemia)
Polymorphonuclear granulocytes (phagocytosis, etc)
neutrophil (60-70%) phagocytosis
here is a picture from our histology course of a neurtophil showing the complex nucleus
chemotaxis after 30-60 min
more synthesized especially in bacterial infection
reset thermostat (pyrogens)
eosinophil (1.5%) phagocytosis
allergic and parasitic inflamation
basophil (0.1%) histamine containing
like mast cells
Mononuclear cells
monocytes (5%) (as in mononucleosis) (phagocytosis)
late chemotaxis become macrophages
alveolar macrophages in lungs
Kupffer's cells in liver
T-cells (80%) (thymus - near heart) cell
(transplant) cytotoxic, suppressor, helper (AIDS)
B-cells (20%) (bone marrow, actually bursa of Fabricius) (become plasma cells)

Triad redness, warmth, swelling
Histamine (from mast cells, platelets)
TRANSPARENCY Fig. 43.5 Inflammation and phagocytosis

SLIDES: blood cells (SEM= scanning electron micrograph))
white blood cell engulfing bacterium (Light Micrograph)
same (SEM)
SLIDES macrophage eating E. coli
macrophage - asbestos
fibrin (2 slides)

There are specific responses to injury

Humoral immunity - B cells
TRANSPARENCY (Fig. 43.4) lymph system and nodes
TRANSPARENCY (Fig. 43.6) clones of plasma cells and memory cells derived from B cells for specific antigens

Interesting continued development through life of monocytes, granulocytes and lymphocytes from stem cells
note, the bone marrow which makes blood cells is mostly in the head and ribs, the two most likely locations for X-rays which are dangerous

Antigen (virus coat, usually not self)
TRANSPARENCY (Fig. 43.14) Antigenic determinant (epitope)

monoclonal antibodies
get B lymphocytes and myeloma cells
get hybridoma cells
screen for hybridoma
select for clone making antibody

Antibody [Tindependent (vs. dependent) antigens]
IgM pentamer, agglutinate
IgG most abundant, monomer, cross placenta
IgA dimer in secretions
IgD on B cells, antigen receptors
IgE allergy, bind to mast cells (histamine)

Rh factor
- mother and + fetus problem if blood crosses over (during delivery)
problem is next time since IgG crosses placenta
treat mother with antibodies (passive immunity) then she will not mount active immunity

Blood groups
Although This topic was covered last semester, it is fundamental and a bit confusing so some points are repeated here.
genotypes IA IA or IA i have phenotype A, A antigens, anti-B antibodies
genotypes IB IB or IB i have phenotype B, B antigens, anti-A antibodies
genotype IA IB has phenotype AB, A and B antigens, no antibodies
genotype ii has phenotype O, no antigens, antibodies to both A and B
O universal donor, AB universal recipient
There are already antibodies since blood group polysaccharides are like those of bacteria even though there was no previous exposure to antigens. IgM not cross placenta

Nonspecific defenses
Complement - 20 proteins - system vasodialtion phagocytosis
coat microorganisms, opsonization
interferon triggers synthesis of antiviral proteins
leukocytosis - inducing factor

Wrap up on humoral immunity TRANSPARENCY (Fig. 43.16)
agglutination, mark for phagocytosis, complement -> cell lysis
TRANSPARENCY Fig. 43.17 show complement better

TRANSPARENCY Fig. 43.8 development of lymphocytes from marrow, thymus

TRANSPARENCY helper T cells [TH] (Fig. 43.11)
antigen presenting macrophage [T-dependent (vs. independent) antigens]

MHC major histocompatability complex 20 genes 50 alleles each
Class II MHC only on macrophages (and B lymphocytes)

cytokines - chemical signals from one cell to another

TRANSPARENCY 43.13 antigen presented by TH to B cell

TRANSPARENCY cytotoxic T cells [TC] (Fig. 43.12)
Class I MHC - actually on lots of cells (infected cells)
[try to match MHC (tissue typing) for transplantation]

summary TRANSPARENCY Fig. 43.10

self vs nonself (auto)immunity
insulin dependent diabetes
rheumatic fever - streptococcal antibodies also to valves
Graves TSH receptors stim excess TH

Dr. Keath is SLU Biology department's immunologist, and she teaches BL A-463 "Foundations of Immunology"

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this page was last updated 2/18/03