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Human Body_TP > Immune System Histology > Flashcards

Immune System Histology Flashcards

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
Q

mast cell function

A

-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
Q

mast cell histology

A

-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
Q

neutrophil function

A

-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
Q

neutrophil histology

A

-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
Q

eosinophil function

A

-granulocytes that primarily mediate the response to parasitic infection and allergens
-release contents of granules through exocytosis

30
Q

what are in the granules of eosinophils?

A

-major basic protein (cytotoxic)
-eosinophilic peroxidase (reactive oxygen species)
-eosinoplilic cationic protein (ribonuclease)
-eosinophil-derived neurotoxin (ribonuclease)

31
Q

eosinophil histology

A

-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
Q

macrophage and monocyte function in immunity

A

-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
Q

macrophage and monocyte role in maintenance of homeostasis

A

iron recycling and bone remodeling

34
Q

macrophage and monocyte histology

A

-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
Q

lymphocyte function

A

-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
Q

function of NK cells

A

-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
Q

function of T cells (cell-mediated)

A

-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
Q

function of B cells (humoral)

A

-antigen-presenting cells
-form memory cells
-produces antibodies

39
Q

lymphocyte histology

A

-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
Q

how are NK cells stained?

A

-Wright’s
-bigger than lymphocytes (15-18 micrometers)
-large nuclei with coarse chromatin
-small granules in cytoplasm
-IHC marker of CD56

41
Q

plasma cell function and histology

A

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
Q

severe combined immunodeficiency (SCID)

A

-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
Q

when do symptoms of SCID appear and what are they?

A

-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
Q

SCID immune system

A

-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
Q

what are the most common types of SCID?

A

-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
Q

SCID treatment

A

most common treatments:
-antibiotics
-immunoglobulin replacement therapy (IVIG)
-patient isolation
-allogenic bone marrow transplant
other treatments:
-enzyme replacement therapy
-gene therapy

47
Q

hashimoto’s overall

A

-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
Q

normal thyroid function

A

thyroid hormone affects:
1. how the body uses energy (metabolism)
2. maintaining body heat
3. supporting organ function (heart, brain, muscles, CNS, GI)

49
Q

hashimoto’s pathophysiology

A

overall: gradual thyroid failure
1. destruction of thyroid gland via autoimmune mechanisms
2. lymphocytic infiltration

50
Q

what does thyroid peroxidase do?

A

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
Q

hashimoto’s diagnosis

A

-elevated levels of thyroid stimulating hormone
-low thyroxine levels
-high anti thyroid peroxidase antibodies
-high anti thyroglobulin antibody

52
Q

what are symptoms of hashimoto’s?

A

-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
Q

how is hashimoto’s treated?

A

levothyroxine- works by replacing normal thyroid hormone that is usually present in the body

54
Q

chronic myeloid leukemia (CML)

A

-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
Q

what are the phases?

A

-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
Q

what are blast cells?

A

immature blood cells that build up in the bone marrow and blood

57
Q

philadelphia chromosome

A

-found in nearly all cases of CML
-reciprocal translocation between chromosomes 9 and 22
-BCR-ABL1 fusion gene

58
Q

what is reciprocal translocation?

A

a genetic rearrangement that occurs when two parts of chromosomes are exchanged, without net loss of genetic info

59
Q

CML pathophysiology

A

-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
Q

CML diagnosis

A

-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
Q

what are some treatments of CML?

A

-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_TP (16 decks)

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