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Immune System Histology Flashcards

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1
Q

what are primary lymphoid organs?

A

-bone marrow and thymus
-central locations for blood and immune cell development

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2
Q

bone marrow

A

-red or yellow bone marrow that are located in the center of most bones
-red marrow contains red blood stem cells
-yellow marrow contains fat

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3
Q

what is bone marrow vasculature composed of?

A

arterioles which transition into a dense network of fenestrated sinusoids

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4
Q

what is the function of bone marrow?

A

bone marrow produces blood cells: red blood cells, white blood cells, and platelets

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5
Q

thymus gland

A

superior mediastinal retrosternal organ split into two lobes with a cortex and medulla

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6
Q

what is the function of the thymus?

A

-development of T cells
-progenitor cells from the bone marrow enter thymic medulla by high endothelial venules (HEVs)

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7
Q

what are secondary lymphoid organs?

A

-where lymphocytes are activated
-lymph nodes, spleen, mucosal-associated lymphoid tissues like tonsils, peyer’s patches, bronchus-associated lymphoid tissues (BALT)
-arranged as series of filters

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8
Q

lymph nodes

A

-bean-shaped, encapsulated clumps of tissue
-contain immune cells
-filter, immune response
-100-200 lymph nodes throughout the body
-swollen or painful lymph nodes —> sign of active immune system

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9
Q

spleen

A

-largest lymphoid organ
-found in the upper left abdomen, beneath the diaphragm
-composed of two tissue types: red pulp with vascular sinuses filled with blood and white pulp with lymphatic tissue
-filter for blood, break down aged red blood cells, and stores/breaks down platelets

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10
Q

mucosa-associated lymphoid tissue (MALT)

A

-dispersed aggregates of nonencapsulated lymphoid tissue within mucosa
-local immune response at the mucosal surface

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11
Q

types of MALT

A

-gut-associated lymphoid tissue (GALT)
-bronchus-associated lymphoid tissue (BALT)
-nasal-associated lymphoid tissue (NALT)

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12
Q

peyer’s patches

A

-large masses of confluent lymphoid particles
-found in lamina propria and submucosa of ileum (part of the small intestine)
-protect against pathogenic growth in the intestine

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13
Q

bronchus-associated lymphoid tissue (BALT)

A

-intrapulmonary lymphoid tissue found in all lobes of the lungs and along the bronchi
-maintenance and regulation of lung mucosal immune homeostasis

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14
Q

circulatory system vs lymphatic system

A

-cardiovascular circulatory system is closed and contains a pump
-lymphatic system is open with no pump and lined with lymphatic endothelial cells (LECs)
-lymphatic drainage is facilitated by interstitial pressure, which is determined by a hydrostatic/oncotic equilibrium

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15
Q

high interstitial pressure —> lymphatic absorption

A

-when the interstitial pressure is greater than lymphatic pressure, fluid diffuses into the initial lymphatics
-facilitated by discontinuous basement membrane on the initial lymphatics

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16
Q

lymphatic absorption

A

initial lymphatics —> pre-collecting lymphatics —> collecting lymphatics

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17
Q

collecting lymphatics: morphology

A

-possess a continuous basement membrane, one-way valves, and SMCs
-muscle contraction drives fluid upstream and creates suction with pre-collecting lymphatics

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18
Q

overview of cells

A

multipotential hematopoietic stem cell (hemocytoblast) —> can become common myeloid progenitor or common lymphoid progenitor

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19
Q

common myeloid progenitor

A

can become a megakaryocyte, erythrocyte, mast cell, myeloblast

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20
Q

common lymphoid progenitor

A

can become a natural killer cell (large granular lymphocyte) or small lymphocyte

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21
Q

stain types

A

-hematoxylin and eosin (H&E)- nuclei stains purplish blue and the cytoplasm and extracellular matrix are pink
-toluidine blue stain- metachromatic properties and mast cell granules
-wright’s stain- mix of eosin and methylene blue, nuclei stains purplish blue, neutrophilic granules stain brown, eosinophilic granules stain red, erythrocytes stain pink, and lymphocyte cytoplasm stains pale blue
-immunohistochemistry- IHC antibody stains either nucleus or cytoplasm of a specific cell type and usually shows up brown but can be other colors

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22
Q

megakaryocytes

A

-largest cell in the bone marrow
-granular cytoplasm
-multinucleated with proplatelet extensions
-responsible for platelet generation- can form thousands of platelets from one cell, proplatelets are the extensions of long cytoplasmic processes, and fragmentation into platelets

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23
Q

megakaryocytes —> thrombocytes

A

-thrombocytes have an immune function
-form blood clots and stop bleeding
-express pattern recognition receptors (PRRs) to bind to pathogens
-cytokine and chemokine release
-can activate macrophages, neutrophils, and dendritic cells

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24
Q

platelets

A

-small
-disk shaped or spikey based on activation
-anucleate
-stain purplish blue in H&E due to granules

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25
mast cell function
-mediate inflammatory response -contain granules loaded with histamine and heparin -when activated, histamine is released -histamine causes the blood vessels to expand and become more permeable ---> leads to redness, warmth, and swelling often seen in allergic reactions
26
mast cell histology
-round or oval shaped 8-20 micrometers -cytoplasm filled with granules -round to oval nuclei -typically found in connective tissue -in toluidine blue stain, the granulocytes are an intense purple color
27
neutrophil function
-granulocytes that have broad antimicrobial properties -phagocytosis- engulfs pathogens, destruction through oxidative reagents -degranulation- antimicrobial peptides (e.g. defensin) and enzymes for production of reactive oxygen species -NETosis- decondense chromatin, secretes from the cell to trap and kill microbes
28
neutrophil histology
-multilobed nucleus (2 or 3-5) -~12-14 micrometer diameter (smaller than eosinophils or macrophages) -cytoplasm pale pink color under H&E -stains for blood smear (e.g. Wright)- pale blue-pink cytoplasm, many granules -in IHC it stains CD66b and myeloperoxidase (MPO)
29
eosinophil function
-granulocytes that primarily mediate the response to parasitic infection and allergens -release contents of granules through exocytosis
30
what are in the granules of eosinophils?
-major basic protein (cytotoxic) -eosinophilic peroxidase (reactive oxygen species) -eosinoplilic cationic protein (ribonuclease) -eosinophil-derived neurotoxin (ribonuclease)
31
eosinophil histology
-bilobed nucleus -~12-17 micrometers in diameter ---> larger than neutrophils, smaller than macrophages -acidophilic granules (stain red or reddish purple) -stains: any stain containing eosin (H&E), congo red (azo dye with pH indicator properties), and IHC markers (antibodies against secreted factors (e.g. major basic protein),IL5Ra, CCR3
32
macrophage and monocyte function in immunity
-antigen presentation with active lymphocytes -phagocytosis where you engulf pathogens, destroy through oxidative reagents -amplification of the immune response by secretion of chemokines and pro-inflammatory cytokines -repair and resolve after inflammation with secretion of anti-inflammatory cytokines and tissue repair factors
33
macrophage and monocyte role in maintenance of homeostasis
iron recycling and bone remodeling
34
macrophage and monocyte histology
-eccentric nuclei, often indented -round to oval shape -large, 10-30 micrometers in diameter -"foamy" looking cytoplasm (secondary lysosomes) -stains: H&E, stains for blood smears like Wright's (pale blue cytoplasm, few granules), and IHC markers (CD68, CD11b, CD14)
35
lymphocyte function
-natural killer (NK) cells, T cells, and B cells -NK cells are involved in the innate immune response -T and B cells are in the adaptive immune response
36
function of NK cells
-recognize 'missing self' on cells where the self are MHC Class I molecules -destroy infected cells with perforin and granzymes -release cytokines to tell other immune cells to help
37
function of T cells (cell-mediated)
-ID specific features of pathogens -helper T cells (CD4+) and cytotoxic T cells (CD8+) -CD8+ will directly kill infected cells via apoptosis -CD4+ will influence other cells via cytokines and cell-cell interactions
38
function of B cells (humoral)
-antigen-presenting cells -form memory cells -produces antibodies
39
lymphocyte histology
-similar in size to red blood cells -spherical nuclei -scant cytoplasm -IHC markers for T cells: CD3, CD4, and CD8 then for B cells: CD19
40
how are NK cells stained?
-Wright's -bigger than lymphocytes (15-18 micrometers) -large nuclei with coarse chromatin -small granules in cytoplasm -IHC marker of CD56
41
plasma cell function and histology
function: -differentiated B cells -secretes immunoglobulin/antibodies in response to antigens histology (wright's): -slightly larger than lymphocytes (14-20 micrometers) -round nucleus with coarse chromatin -abundant deep blue cytoplasm -IHC marker of CD138 -paler part of the cytoplasm near the nucleus
42
severe combined immunodeficiency (SCID)
-group of rare inherited disorders that cause infants to be born without a working immune system -SCID infants appear healthy at birth but become highly susceptible to severe infections
43
when do symptoms of SCID appear and what are they?
-present at < 3 months of age -failure to thrive -recurrent bacterial, viral, fungal, and protozoal infections -chronic diarrhea -thrush in mouth and diaper area -seborrheic dermatitis -alopecia -absent lymphatic tissue, including tonsils and thymus
44
SCID immune system
-SCID affects both the B and T arms of the adaptive immune system -newborn screening test- measures T cell receptor excision circles (TRECs), a byproduct of T cell development
45
what are the most common types of SCID?
-X-linked SCID- low levels of T cells and natural killer cells (NK cells) due to defective regulatory T cell development -recombinase activating genes 1 and 2 (RAG1/2) SCID- no T and B cells due to missing lymphocyte receptor formation -adenosine deaminase (ADA) deficiency SCID- low levels of T, B, and NK cells due to toxic metabolite
46
SCID treatment
most common treatments: -antibiotics -immunoglobulin replacement therapy (IVIG) -patient isolation -allogenic bone marrow transplant other treatments: -enzyme replacement therapy -gene therapy
47
hashimoto's overall
-autoimmune disease causing destruction of thyroid cells ---> decreased production of thyroid hormone (hypothyroidism) -chronic autoimmune thyroiditis or chronic lymphocytic thyroiditis -caused from genetic and environment -
48
normal thyroid function
thyroid hormone affects: 1. how the body uses energy (metabolism) 2. maintaining body heat 3. supporting organ function (heart, brain, muscles, CNS, GI)
49
hashimoto's pathophysiology
overall: gradual thyroid failure 1. destruction of thyroid gland via autoimmune mechanisms 2. lymphocytic infiltration
50
what does thyroid peroxidase do?
thyroid peroxidase and thyroid globulin ---> block the function of the antigens ---> damage thyroid ---> get inflammation of the thyroid ---> overtime the thyroid gland gets bigger and damaged and can't make thyroid hormone
51
hashimoto's diagnosis
-elevated levels of thyroid stimulating hormone -low thyroxine levels -high anti thyroid peroxidase antibodies -high anti thyroglobulin antibody
52
what are symptoms of hashimoto's?
-larger thyroid gland -exhaustion -weight gain -muscle weakness -constipation -dry skin and hair -epithelial thinning -slowed hair growth -increase vascular resistance in periphery and reduced cardiac output
53
how is hashimoto's treated?
levothyroxine- works by replacing normal thyroid hormone that is usually present in the body
54
chronic myeloid leukemia (CML)
-cancer of the bone marrow and blood -10% of all new leukemia cases ---> 50% of newly diagnosed patients are asymptomatic -slowly progressing usually presents during or after middle age
55
what are the phases?
-chronic- the earliest phase with best response to treatment -accelerated- transitional phase where the disease becomes more aggressive -blast- severe, aggressive phase becoming life-threatening
56
what are blast cells?
immature blood cells that build up in the bone marrow and blood
57
philadelphia chromosome
-found in nearly all cases of CML -reciprocal translocation between chromosomes 9 and 22 -BCR-ABL1 fusion gene
58
what is reciprocal translocation?
a genetic rearrangement that occurs when two parts of chromosomes are exchanged, without net loss of genetic info
59
CML pathophysiology
-BCR-ABL1 oncogene (abnormally expressed or mutated genes that cause cancer by inducing cells to grow and divide uncontrollably) -constitutively active tyrosine kinase (enzymes responsible for the activation of many proteins by signal transduction cascades) -granulocyte over-proliferation -extra cells in blood and bone marrow
60
CML diagnosis
-leukocytosis (high WBC)- anemia (low RBC) in advanced disease -bone marrow biopsy (cytogenic analysis with detection of the philadelphia chromosome) -fluorescence in situ hybridization or qPCR for detection of the BCR-ABL gene -reverse transcriptase for detection of the BCR-ABL protein
61
what are some treatments of CML?
-TKI inhibitors- target the tyrosine kinase protein from the BCR-ABL gene -chemotherapy- combined with targeted therapy for aggressive CML -bone marrow transplants- only treatment that can cure CML but high risk and rate of serious complications

Human Body (25 decks)

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