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Department of Natural SciencesUniversity of St. La Salle
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� They have fewer cells that are set apart due to anabundance of intercellular substance or ground
substance which contains fibers.
� The different contents of intercellular substance,
CT cells and fibers account for the difference inappearance of the various CT.
� Except in a few CT types (mucous and cartilage),
there are blood vessels, lymphatics and nerves
found in the ground substance.
� The physical properties of CT allow it to bind, fillspaces, and to separate functional units of other
tissues and organs, allowing maintenance and
coordination of all body functions.
GENERAL CHARACTERISTICS
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All CT celltypes are
derived from
cells of
embryonic
mesenchyme
originating
from theembryonic
mesoderm.
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In any type of CT, there are 3 basic elements
to consider.
CT types and subtypes are classified
according to the amount, types, and
proportions of these 3 components:
1.Ground substance- forms the extracellularmatrix together with tissue fluid (bound
water of solvation) and protein fibers; maybe
fluid, gelatinous or solid
2.Fibers- maybe white or collagenous, yellowor elastic, reticular or argyrophyl
3.CT cells- of several types, mobile wandering
or relatively fixed elements
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� This abundant intercellular substance vary in
consistency from a thin fluid to a hard,
calcareous substance.
� The formed elements of CT are embedded in
this matrix of amorphous, colorless,
transparent material with the properties of a
viscous solution or thin gel.
� It is the medium through which all nutrients
and waste products must pass in transit between the blood and parenchymal cells of
the organs.
� It consists mostly of tissue fluids, salts and 2
classes of glycoconjugates:
GROUND SUBSTANCE
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1.PROTEOGLYCANS-
composed of a core protein
to which glycosamino-
glycans (GAGs) are
attached. GAGs are straight-
chain polymers of repeating
sugar heterodimers made up
of hexosamine and uronic
acid.
2.Five major classes of GAGs exist in CT: hyaluronic acid
(does not form proteoglycans, and determines the
structural and physiological characteristics of ground
substance), chondroitin sulfate, dermatan sulfate, keratan
sulfate, and heparan sulfate.
� Lysosomal enzyme deficiencies for degradation of GAGs
lead to their accumulation, resulting to several human
disorders e.g., Hurler syndrome, Hunter syndrome,
Morquio syndrome
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ECM of mouse endometrium after
fixation in the presence of Safranin O. A network of
proteoglycans fills the intercellularspaces. Some proteoglycan
filaments are in close contact withthe cell surface (arrows).
Schematic diagram of cell-surface
proteoglycan. The core proteinspans the plasma membrane
through the cytoplasmic domain.The proteoglycans possess 3
heparan sulfate chains andsometimes chondroitin sulfate.
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2.GLYCOPROTEINS- globular proteins to which
shorter, branched oligosaccharide chains are
covalently bound.� These so-called adhesion
glycoproteins mediate
attachment of cells to their
matrix, influence the state
of differentiation of cells,
and organization of their
cytoskeleton.
� Examples: Fibronectin- long flexible molecule with
cell-binding, collagen-binding, GAG-binding, andcytoskeleton-binding domains along their length;
cell surface receptors are called integrins; plasma
fibronectin synthesized by liver and endothelial cells
binds to fibrin during blood clotting reactions
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Laminin- binds to membranes of epithelial and muscle
cells, to type-IV collagen, and heparan sulfate;
significant in the assembly of the basal lamina,influencing the form and function of epithelial cells
Thrombospondin- activated platelet-product; binds to
fibrinogen, plasmalogen and its activator; a participant
in blood clotting; function is poorly understood
Chondronectin- a component of cartilage matrix that mediates attachment of chondrocytes to their matrix
Fibrillin- a nonsulfated glycoprotein speculated to be
essential for normal development. It is often associated
with elastic fibers or with epithelial basal laminae
Marfan syndrome is due to a defective fibrillin geneon chromosome 15, characterized by excessively
long arms and legs and progressive dilatation and
fatal rupture of the ascending aorta (Pres. Abraham
Lincoln).
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A: The structure of fibronectin.
Fibronectin is a dimer bound by
S³S groups, formed by serially
disposed coiled sites, that bind to
type I collagen, heparan sulfate,
other proteoglycans, and cell
membrane receptors.
B: The structure of laminin,which is formed by 3 intertwined
polypeptides in the shape of a
cross. There are sites on the
molecule with a high affinity for
cell membrane receptors andtype IV collagen and heparan
sulfate, which are components of
basal laminae. Laminin thus
promotes adhesion of cells to
basal laminae.
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Transverse section of
mouse endometrium.Immunocytochemical
staining shows the
distribution of fibronectin in
the endometrial stroma.
Transverse section of tongue.
Immunocytochemical stainingshows the distribution of
laminin basement
membranes in epithelial layer,
capillary blood vessels, nerve
fibers, and striated muscle.
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� GAGs in CT are highly sulfated which attracts water of
hydration. If fluid is injected into CT, it remains localized,
walled off by a viscous ground substance.� This property acts as barrier to the spread of bacteria that
gains access to the tissues.
� Some bacteria secrete hyaluronidase (Staphylo/ Strepto/
Pneumococci), and collagenase (Clostridium perfringens)
that breakdown matrix components.� EDEMA is a condition characterized by accumulation of
excess tissue fluid.
� The water in tissue fluid is forced out by hydrostatic
pressure from the arterial end.
� Loss of fluid to the tissues increases the colloid osmoticpressure, and draws most of the fluid back into the blood.
� Excess fluids remaining in tissues is normally drained
away by lymphatic capillaries, so that there is no net
change in the amount of blood or tissue fluid.
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Edema accompanies pathological conditions that
cause:
Increased hydrostatic pressure in capillaries byobstructing venous blood flow (e.g. congestive
heart failure)
Decreased colloid osmotic pressure in the blood
caused by lack of blood proteins (e.g. starvation)
Increased hydrostatic pressure in the tissuecaused by blockage of lymphatic drainage by
parasites or tumor cells
Increased colloid osmotic pressure in the tissue
caused by excessive accumulation of GAGs in
the matrix.
Hypothyroidism resulting
from this condition is
referred to as myxedema.
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1.COLLAGEN FIBERS
� Principal producers are fibroblasts; epithelial and smoothmuscle cells also secrete their own type-IV collagen.
� Most numerous CT matrix, running in all directions in a
wavy course; dull and opaque in appearance.
� Fibers bundled together branch and anastomose;
individual fibers do not branch.� With the EM, unit fibrils of collagen show periodic cross
striations every 67 nm of their length.
CONNECTIVE TISSUE FIBERS
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Unit fibrils are made up of 3 polypeptide chains
(E-chains) held together by hydrogen bonds.
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� Collagen occurring in
bundles, or as individual
fibrils, exhibit acidophilic
properties in H & E
stained sections.
� In sections stained with
Massons·s trichome, they
stain green, blue with
Mallory·s trichome stain.� Thin fibers (type III) stain
darkly with silver stains,
but thicker bundles do
not.
� Collagen that do not form
fibers (type IV) cannot be
distinguished from the
surrounding ground
substance except by
immunohistochemistry.
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1.INTRACELLULAR ² free polysomes reading collagen mRNA
attach to the rER, and protocollagen or precollagen-chainsare deposited in the cisternae. Each chain has about 250
amino acids; every 3rd amino acid is glycine.
� The signal peptide is clipped off. Proline and lysine residues
within the chains are then hydroxylated in the ER to form
hydroxyproline and hydroxylysine (unusual amino acidspresent in large amounts in collagen).
� Core sugars (galactose and glucose) attach to the
hydroxylysine residues in the ER.
� Each chain is synthesized with an extra length of peptides
known as registration peptides, which ensure that the
appropriate chains assemble in their correct position in the
resulting triple helical molecule called procollagen.
� Further glycosylation may occur in the Golgi complex, where
procollagen is packaged for secretion. Golgi vesicles release
procollagen into the extracellular space by exocytosis.
Synthesis and Assembly of Collagen
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2.EXTRACELLULAR- in the extra
cellular space, the enzyme
procollagen peptidase cleavesthe registration peptides from
procollagen, converting it to
tropocollagen. Catalyzed by
lysyl oxidase, these become
aligned in staggered fashion to form collagen fibers, possibly
under the control of adjacent
fiber-producing cells.
� The turnover of collagen is
slowest in tendons, fastest inloose CT. Macrophages and neutrophils break down old
collagen, and replaced by fibroblasts.
� As humans age, extracellular collagen becomes
increasingly cross-linked, & turn-over slows down in CT.
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COLLAGEN TYPES- fibril-forming (I,II,III,V,XI), fibril-
associated (IX, XII), network-forming (IV), anchoring
(VII):
� Type I- most abundant and widespread, forms large
fibers and fiber bundles. It is found in tendons,
ligaments, bone, dermis, organ capsules, and loose CT.
� Type II- form only very thin fibers; found in embryonic
notochord; in adults, only in the nucleus pulposus of the
intervertebral disk, vitreous body of the eye, and in the
hyaline and elastic cartilage matrix.
� Type III- similar to type I, but is more heavily glycosylated
and stain with silver.
� Often found in association with type I, these reticular
variety forms networks of thin fibrils that are
abundant in loose CT, in soft and compliant organs
such as the walls of blood vessels, in the stroma of
spleen, kidney and uterus, and compose the reticular
laminae underlying epithelial basal laminae.
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Collagen types I, II, and III are called interstitial
collagens which form microscopically visible
fibers.
� Type IV- does not form fibers or fibrils; major
collagen type found in basal laminae.
� Type V- present in external lamina of muscle
fibers, epithelial basal lamina, blood vessels andin small amounts elsewhere
� Type VI- present where types I and III are found;
kidney, uterus, cornea.
� Type VII- largest of the collagen family; formanchoring fibrils of epithelial basal lamina,
serving to stabilize and firmly anchor the
epithelium to the dermis.
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� Type VIII- secretory product of endothelial cells;
a major component of Descemet·s membrane,
the corneal epithelium basal lamina.� Type IX- found mainly in cartilage; maintains the
3-D arrangement of type II fibrils by serving as
coupler in their sites of intersection
� Type X- found in the matrix surrounding
hypertrophic chondrocytes of degenerating
growth plate cartilage in sites of future bone
formation.
� Type XI (cartilage) and XII (tendon fibroblasts)-
very poorly understood types
Weight for weight, collagen tensile strength
is greater than that of steel.
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� Chemical Characteristics- easily stained byordinary dyes; yield gelatin when boiled; dissolve
easily in boiling dilute acids and alkali; easily
digested by artificial gastric juice; resistant to
solutions of alkaline pancreatic juice.� Cortisol (hydrocortisone) produced by adrenal
glands under the influence of ACTH inhibits CT
fiber synthesis and retards local inflammatory
and immune responses by CT cells.� Cortisol reduces local heat, redness and
tenderness, but delay and impair wound
healing.
Histophysiology of Collagen
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� Because collagen synthesis depends on the expression of
several genes and on several post-translation events,
many human diseases are associated with faulty collagensynthesis. Examples:
� Progressive systemic sclerosis- excessive
accumulation of collagen (fibrosis) in almost all organs;
� Keloid- local swelling caused by abnormal amounts of
collagen that form in scars of skin;� Ehlers-Danlos type IV- aortic/ intestinal rupture due to
faulty transcription of collagen type III;
� Ehlers-Danlos type VII- increased articular motility due
to decreased procollagen peptidase activity;
� Scurvy- ulceration of gums, hemorrhages due to lackof Vit. C, a cofactor for proline hydroxylase;
� Osteogenesis imperfecta- spontaneous fractures &
cardiac insufficiency due to mutation in collagen type I
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Section of a muscular artery stained with picro-sirius andobserved with polarization optics. The upper tunica media
(muscular layer) contains reticular fibers consisting mainly of
collagen type III. The lower layer (tunica adventitia) contains
thick fibers and bundles of collagen type I. Deficiencies of
collagen type III may result in rupture of the arterial wall
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2. YELLOW or ELASTIC FIBERS
� Form gentle curves or spirals at their free ends
when released from tension� Do not form bundles; individual fibers branch and
anastomose to form networks
� They can be stretched to 150% of their length
without breaking, but lose their resiliency withadvancing age.
� Appears yellowish, highly refractile, homogenous
and are not made up of fibrillar subunits that are
visible with the light microscope.� Composed of 2 elements: microfibrils, aggregated
in bundles which are embedded in abundant and
amorphous elastin.
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Each fibril is made up of still smaller fibrils united by
a small amount of ground substance. These smaller
´microfibrilsµ have periodic cross bandings.
Ground substance stains with PAS due to its protein-
polysaccharide content: mucopolysaccharides,
hyalurinate, chondroitin sulfates.
Chemical characteristics:Stains poorly with standard ionic dyes since it
contains a few charged amino acids; as such it
requires the special Verhoeff·s (Weigerts· resorcin
fuschin) stain or Halmi·s aldehyde-fuchsin method.
It does not yield gelatin on boilingDoes not easily dissolve in boiling dilute acids and
alkali; and easily digested by pancreatic juice which
contains elastase.
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In this side by side comparison of fibrous and elastic tendons cut in
cross-section, the relative sizes of fibers is compared. Notice how
large and robust the collagen fibers are compared to the smaller
elastic types. Nuclei of fibroblasts visible along the edges of fibers
are a good indicator these are tendons in cross-section.
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1.Intracellular- microfibrillar proteins containing
mostly hydrophilic amino acids, and proelastin(contains large amounts of the hydrophobic amino
acids glycine, proline and valine, thus accounting for
elastin·s insolubility) are synthesized on rER and
secreted separately.
2.Extracellular- proelastin molecules polymerizeextracellularly to form elastin chains.
� Lysyl oxidases then catalyze the conversion of
certain lysine residues of elastin to aldehydes, 3
of which condense with a 4th unaltered lysine
residue to form desmosine and isodesmosine.
� These very rare amino acids found in elastin
cross-link individual chains, which then associate
with numerous microfibrils to form a branching
and anastomosing network of elastic fibers.
Synthesis and Assembly of Elastin:
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Skin dermis, selectively stained for elastic fibers. Dark
elastic fibers are interspersed with pale red collagen
fibers. The elastic fibers are responsible for skin·selasticity . Elastin molecules are joined by covalent
bonds to generate an extensive cross-linked network.
Because each elastin molecule in the network can
expand and contract like a random coil, the entire
network can stretch and recoil like a rubber band.
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A: Rat mesentery showing
nonanastomosing bundles
of collagen fibers, whilethe elastic fibers appear as
thin, dark anastomosing
fibers. Collagen and elastic
fibers provide structure
and elasticity, respectively,to the mesentery.
B: The same preparation
observed with polarizing
microscopy. Collagen
bundles of variousthicknesses are observed.
In the superimposed
regions, the bundles of
collagen are a dark color.
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3.ARGYROPHYL or RETICULAR FIBERS
� Fibers are not branched, and are not so wavy as the
collagenous fibers when released from tension.� They are chemically identical to collagen, hence
these fibers are considered as precursors of type I
and III collagen; however, they are thinner and form
delicate networks instead of thick bundles
� Chemical characteristics- show affinity to silver(black) stains, hence argyrophyl; do not yield gelatin
on boiling; not easily dissolved by dilute acids and
alkali; not so easily digested by gastric juice; not so
resistant to solutions of alkaline pancreatic juice.
� Distribution- abundant in regions around blood
vessels, muscle fibers, fat cells, basement membrane
of epithelia, endoneurium, lymphoid organs and red
bone marrow.
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Section of an adrenal cortex, silver stained to show reticular
fibers. This is a thick section made to emphasize the networks
formed by these fibers, which consist of collagen type III. Nuclei
are black, and cytoplasm is unstained.
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1. FIXED CELLS
a. Mesenchymal cells- these cells have multipledevelopmental potentialities, differentiating along
several different lines to produce many different kinds
of CT cells, smooth muscle cells, blood cells.
� They disappear when component cells undergo
differentiation.� Embryonic mesenchyme
consists of a loose network
of stellate mesenchymal
cells and abundant
intercellular fluid.� Undifferentiated mesen-
chymal cells remain in adult
CT as reserve cells called adventitial cells, which are
difficult to distinguish from some fibroblasts.
CONNECTIVE TISSUE CELLS
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b.Fibroblasts (fibrocytes or
desmocytes)
� Flattened cells with a finelygranular cytoplasm and a
vesicular nucleus.
� Young fibroblasts are stellate
cells with long cytoplasmic
processes and a large, ovoid,pale-staining nucleus with
nucleoli and sparse chromatin.
� They have long, slender mitochondria extending into
the processes, presence of ER and well-developedGolgi complex, a sign of active protein synthesis.
� Cytoplasm appears acidophilic but becomes slightly
basophilic when actively synthesizing ground
substance
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� The smaller, mature type ( fibrocytes) are less active,
spindle-shaped with a dark, elongate nucleus and
fewer cytoplasmic organelles.� They can revert to the fibroblast stage and participate
in tissue repair.
� Differentiated cells ordinarily do not give rise to other
CT cell types. They are suspected to become adiposeor bone-forming cells, but it is debatable whether it is
actually the fibroblasts or their undifferentiated
mesenchymal progenitors that undergo these
transformations.
� In other locations, fibroblasts can take on different shapes and acquire additional functions (e.g.,
intestinal villi, interstitial cells of renal papillae,
periniurium of peripheral nerves)
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Fibroblasts actively engaged in synthesis (left) are richer in
mitochondria, lipid droplets, Golgi complex, and rER than
are quiescent fibroblasts or fibrocytes (right).
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c.Reticular Cells
� These make us a functionally
diverse yet morphologicallysimilar group. They produce
the reticular fibers that form
the netlike stroma of hema-
poietic & lymphoid tissues.
� They can phagocytoseantigenic materials and
cellular debris. Others collect antigens on their
surfaces and help activate immunocompetent cells.
� They are typically stellate with long, cytoplasmic
surfaces, with a central, pale, irregularly rounded
nucleus and a prominent nucleolus. The number of
mitochondria, rER and Golgi complex is variable; less
developed organelles maybe stem cells of various
blood types.
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d.Fat or Adipose Cells
� These conspicuous cells are a normal component of
areolar tissue occurring singly or in clumps alongsmall blood vessels. If they accumulate in large
numbers, the tissue is transformed into adipose tissue.
� These are fixed cells containing fat globules in the
cytoplasm. They accumulate so much lipid that the
nucleus is flattened and displaced to one side, thecytoplasm so thinned that it appears as a narrow rim
around the edge of the single large lipid droplet giving
the cell the characteristic signet ring appearance.
� Individual cells are surrounded by a fine network of
reticular or argyrophil fibers.
� The biggest CT cell while all the others are small and
thus are difficult to demonstrate in ordinary slide
preparation.
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� In fresh or formalin-fixed tissue,
the fat droplet can be stained
with osmic acid, but in most histological preparations, the
lipid has been extracted, leaving
only the plasma membrane.
� Fat cells are fully differentiated
and incapable of mitotic division.� The fat cells of the brown fat tissue prominent in
hibernating animals do not contain one big fat globule
but usually several small fat droplets with some
brownish pigment granules.
� In starvation and malnutrition, the fat content of the
fat cells disappears; the cytoplasm becomes more
abundant, serous in character with very tiny fat
droplets. These cells are termed serous fat cells.
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2.FREE, MOBILE or WANDERING CELLS:
a.Macrophages (phagocytes, clasmatocytes,
histiocytes, resting wandering cells or rhagiocrinecells)
� These are large, irregularly shaped cells in loose CT
with vacuoles and abundant cytoplasm, abundant
lysosomes, well-developed Golgi complex, and
protruding pseudopods.� They are infrequent in CT
where blood vessels are few;
being abundant in richly
vascular areas; life spanis about 2 months.
� Maybe either fixed (resident)
or resting, attached to fibers
or free in the ground substance.
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� Fixed macrophages are inactive and
immobile; they are elongated or
stellate shaped.� The fixed variety becomes the
rounded and motile free (elicited)
macrophages when mobilized at the
site in response to a stimulus; the
latter become activatedmacrophages when presented with
phagocytic and antigen-processing
activity.
� These phagocytes help maintain the
integrity of CT by removing foreignsubstances and cellular debris, and
participate in the immune response
by presenting phagocytosed antigens
to lymphocytes and plasma cells.
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Section of rat
skin showing
multinuclear
giant cells
surrounded
by
macrophages
� They may form closely packed masses forming
epithelioid cells. In chronic infection, they may fuse to
form multinucleated foreign body giant cells around foreign objects that are too large or resistant to be
engulfed and destroyed.
� The cell enlarges during phagocytosis, the Golgi net
becomes prominent and the lysosomes discharge
enzymes into the vacuoles.
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� The MONONUCLEAR PHAGOCYTE SYSTEM (formerly the
reticulo-endothelial system) is a group of widely
dispersed cells types that are related by theirmorphology, phagocytic functions and a common origin.
The phagocytic cells in all of the tissues and organs are
derived from precursors in the bone marrow, thru blood
monocytes.
� They all take up vital dyes, react positively for peroxidase,esterase and other lysosomal enzymes, and all have
surface receptors for IgG and complement.
� This system is composed of free or fixed macrophages of
CT (histiocyte), liver (stellate cells of Kupffer), pulmonary
alveoli, lymph node, spleen, bone marrow, serous cavity(pleural and peritoneal macrophages aggregated in small
patches known as ´milky spotsµ), bone (osteoclasts),
nervous system (microglia of the CNS), skin (histiocyte),
synovia (type A cell), tissue macrophages
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b.Mast Cells- large, round or ovoid cells
resembling the basophils of the blood, with pale-
staining nuclei and large basophilic granulesobscuring the nuclei.
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b.These granules are easily soluble in water and
seldom seen in the specimen. The granules contain
pharmacologically active substances such as:
� Heparin- anticoagulant and antiagglutinant
� Histamine- together with leukotrienes and the
eosinophilic chemotactic factor (ECF-A), its
release is responsible for the allergic response to
some foreign proteins or anaphylaxis. Histaminerelease during massive degranulation of mast
cells of anaphylaxis results to increased capillary
permeability with leakage of plasma into tissues,
dramatic fall in blood pressure, unconsciousness,
and even death.� Serotonin- a vasoconstrictor that increases the
permeability of capillaries and venules, having a
marked effect upon blood pressure.
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Mast-cell secretion. 1: IgE molecules are bound to the surface receptors.
2: After a 2nd exposure to an antigen (e.g, bee venom), IgE molecules
bound to surface receptors are cross-linked by the antigen. This
activates adenylate cyclase & results in the phosphorylation of certain
proteins. 3: At the same time, Ca+2 enters the cell. 4: These events lead
to intracellular fusion of specific granules & exocytosis of their contents.5: In addition, phospholipases act on membrane phospholipids to
produce leukotrienes. The process of extrusion does not damage thecell, which remains viable and synthesizes new granules. ECF-A,
eosinophil chemotactic factor of anaphylaxis.
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c.Plasma Cells� Spherical cells with an eccentric
´clock-faceµ nucleus resulting from
a large, central nucleolus & severallarge heterochromatin clumps
regularly spaced inside the nuclear
envelope.
� EM show the presence of an
extensive ER associated withribosomes or RNP granules which
are involved in the synthesis of
antibodies. The secreted proteins
do not aggregate into secretory
granules.� The cytoplasm has well developed Golgi complex and
centrioles, finely granular and intensely basophilic.
� They possess a slight amoeboid motility and are not
actively phagocytic.
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� This cell type arise by further differentiation
of B lymphocytes
� Has a very important function in resistance todisease and is now known to be the principal
producer of antibodies, the immune globulins
of the blood that participate in the body·s
humoral defenses against bacterial infection.� These cells are abundant in the mucous
membrane of GI tract.
� When they disintegrate, their cytoplasmic
inclusions (believed to be products of defective antibody synthesis) are set free and
become acidophilic in staining, termed the
Russell granules or bodies.
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Portion of a chronically inflamed intestinal villus. The plasma cells
are characterized by their size and abundant basophilic
cytoplasm (rER). A large Golgi complex (arrows) is where the
terminal glycosylation of the antibodies (glycoproteins) occurs.
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d. Leukocytes- wandering cell types that originate in the bone
marrow and are carried to CT by the blood and lymph.
� Lymphocytes ² production of immunocompetent cells;
may originate in CT and remain there. However, they mayenter the circulation at any time.
� Eosinophil- abundant in lactating breast and of the
respiratory and alimentary tracts. They accumulate in
the blood and in the tissues in certain allergic, parasitic
infections and sub-acute inflammatory conditions. Theycontain a slight amount of histamine.
� Basophil- contain the anticoagulant heparin, which
prevents blood from clotting too quickly; the vasodilator
histamine; found in sites of exoparasite infection; and
where allergic reactions are occurring
� Neutrophil- generally escapes into CT from capillaries
only in regions of inflammation.
� Monocytes- are rarely seen; are considered as
phagocytes because they may become amoeboid and
show inclusions that stain supravitally with neutral red.
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Section of an inflamed intestinal lamina propria. Inflammation
was caused by nematode parasitism. Aggregated eosinophils
and plasma cells function mainly in the connective tissue by
modulating the inflammatory process.
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