Ganong's Review of Medical Physiology, 23rd Edition

Fibrin clot
Macrophage
Neutrophil
TGF-β1
Platelet
TGF-α
plug
FGF
VEGF
PDGF BB
TGF-β1
IGF
PDGF AB
Blood vessel
FIGURE 3–13 Cutaneous wound 3 days after injury, showing
the multiple cytokines and growth factors affecting the repair
process. VEGF, vascular endothelial growth factor. For other abbreviations,
see Appendix. Note the epidermis growing down under the fibrin
clot, restoring skin continuity. (Modified from Singer AJ, Clark RAF:
Cutaneous wound healing. N Engl J Med 1999;341:738.)
and scar formation. Plasmin aids healing by removing excess fibrin.
This aids the migration of keratinocytes into the wound to
restore the epithelium under the scab. Collagen proliferates,
producing the scar. Wounds gain 20% of their ultimate strength
in 3 weeks and later gain more strength, but they never reach
more than about 70% of the strength of normal skin.
Change in plasma concentration (%)
VEGF
30,100
30,000
700
600
500
400
300
200
100
Neutrophil
FGF-2
C-reactive protein
Serum amyloid A
Haptoglobin
C3
Fibroblast
FGF-2
Fibrinogen
0
Albumin
Transferrin
0 7 14 21
Time after inflammatory stimulus (d)
FIGURE 3–14 Time course of changes in some major acute
phase proteins. C3, C3 component of complement. (Modified and
reproduced with permission from Gitlin JD, Colten HR: Molecular biology of acute
phase plasma proteins. In Pick F, et al [editors]: Lymphokines, vol 14, pages 123–153.
Academic Press, 1987.)
CHAPTER 3 Immunity, Infection, & Inflammation 77
CHAPTER SUMMARY
■ Immune and inflammatory responses are mediated by several
different cell types—granulocytes, lymphocytes, monocytes,
mast cells, tissue macrophages, and antigen presenting cells—
that arise predominantly from the bone marrow and may circulate
or reside in connective tissues.
■ Granulocytes mount phagocytic responses that engulf and destroy
bacteria. These are accompanied by the release of reactive
oxygen species and other mediators into adjacent tissues that
may cause tissue injury.
■ Mast cells and basophils underpin allergic reactions to substances
that would be treated as innocuous by nonallergic individuals.
■ A variety of soluble mediators orchestrate the development of
immunologic effector cells and their subsequent immune and
inflammatory reactions.
■ Innate immunity represents an evolutionarily conserved, primitive
response to stereotypical microbial components.
■ Acquired immunity is slower to develop than innate immunity,
but long-lasting and more effective.
■ Genetic rearrangements endow B and T lymphocytes with a vast
array of receptors capable of recognizing billions of foreign
antigens.
■ Self-reactive lymphocytes are normally deleted; a failure of this
process leads to autoimmune disease. Disease can also result
from abnormal function or development of granulocytes and
lymphocytes. In these latter cases, deficient immune responses
to microbial threats usually result.
MULTIPLE-CHOICE QUESTIONS
For all questions, select the single best answer unless otherwise directed.
1. In normal human blood
A) the eosinophil is the most common type of white blood cell.
B) there are more lymphocytes than neutrophils.
C) the iron is mostly in hemoglobin.
D) there are more white cells than red cells.
E) there are more platelets than red cells.
2. Lymphocytes
A) all originate from the bone marrow after birth.
B) are unaffected by hormones.
C) convert to monocytes in response to antigens.
D) interact with eosinophils to produce platelets.
E) are part of the body’s defense against cancer.
3. The ability of the blood to phagocytose pathogens and mount a
respiratory burst is increased by
A) interleukin-2 (IL-2).
B) granulocyte colony-stimulating factor (G-CSF).
C) erythropoietin.
D) interleukin-4 (IL-4).
E) interleukin-5 (IL-5).
4. Cells responsible for innate immunity are activated most commonly
by
A) glucocorticoids.
B) pollen.
C) carbohydrate sequences in bacterial cell walls.
D) eosinophils.
E) cytoplasmic proteins of bacteria.