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Lymphocytes, Plasma cell myeloma, T cell need enter thymus to get mature …
Lymphocytes
cellular immunity center is T cell (CD4+, CD8+), to kill infected cells. T helper cells at there called Th2.
Humoral immunity center is B cells produce antibodies. B cells activate T help cell, and then the T help cells activate B cells.
Lymphocytosis: primary organs is antigen independent. thymus, and BM are virgin lymphs. Secondary organs: antigen dependent: spleen, lymph nodes, GI associated lymphoid tissue. High % in children.
NK lymphocytes: large granular lymphocytes but lack t cell receptor. 1. innate immunity: no need recognized antigen and kill target cells by injected granules. 2. adaptive immunity involvement: ADCC: antibody dependent cellular cytotoxicity; target cell of antigen + antibody + NK by nk cell cd 16 Fc receptors bound and inject granules.
Plasma cell myeloma
pathogenesis
expanding plasma cell mass: increase in the number or proportion of plasma cells within a particular tissue, usually in the bone marrow.
overproduction of Ig: increase monoclonal gammopathy to increase hypervisccity- suppress normal Ig production, Bence Jones protein (free light chain detective in urine), amyloidosis (accumulate on organs to casue organs function abnormal), autoimmune occurrence, bleeding disorders (targeting, plotting factors interfering )and cryoglobulins, cryoglobulinemia
producation of osteoclast activating factors and cytokines: IL-6 induces proliferation of plasma cell & stimulates osteoclasts' activity
hypercalcemia
CRAB
MGUS
Plasma cell neoplasms
B lymphocytes
end stage is plasm cell-- produce ig
medulla, which is comprised of B cells and plasma cells.
1 plasm cell--1 antibody with one light chain,one heavy chain
abnormal plasma cell--abnormal single homogenous Ig called paraprotin or M protein-- unbalanced production of light chains and heavy chains. BM
Monoclonal gammopathy of undetermined significance
asymptomatic. gradual increase of the m protein that monoclonal antibodies < 30g/dl, but BM plasma cells< 10%. Hence do not infiltrate the bone marrow extensively
No CRAB: No hypercalcemia, renal insufficiency, anemia, bone lytic lesions
also called multiple myeloma. >10%
increase serum monoclonal protein, skeletal destruction with osteolytic lesions, fractures, bone pain, hypercalemia, anemia.
site: most active hematopoiesis involvement: proximal end of large bone, sternum, axial skeleton, lliac crest.
T cell need enter thymus to get mature , so thymus is primary lymphoid organs
Nomral T cell has no lymphocytes. if has, it is cytotoxic T cells or NK.
thymus cortex: maturation , rearrangement, apoptosis, subdivide to CD4 --T. Helper, CD 8--cytotoxic
T helper: CD4- Cell mediated immunity, Have granules.
Regulatory T cells: also called T suppressor to suppress activation of own immune system, has granules.
cytotoxic: CD8 to kill cells that virally infected, have granules.
Thymus medulla: navie T cell under undergoes lymphopoiesis , further apotosis
Mature lymphoid neoplasms: called Non-Hodgkin Lymphomas- NHL
mature lymphoid neoplasma has no Reed-sternberg cell
young cell markers--acute lymphocytic leukemia., mature cell markers: NHL
The majority of B cell type, >99%
T cell is mostly CD4+
Hodgkin's Lymphoma
large malignant Reed-Sternberg cells or RS variants with an
appropriate cellular background of a proliferative benign inflammatory cells
2 large nuclei that looks like the eye of the owls.
characteristics: arise lymph node of cervical region, majority in young (15-35 yrs), Reed-Sternberg , the tumor cell are surrounded T lymphocytes in a rosette like manner
B cells under steers differentiation defective--reed sternberg cells that has bilobed nucleus: eosinophilic nucleoli
Lymph node
3 layers
cortex is B cell
primary follicles: in site lymohocytes are no exposed to the antigens
Secondary follicles: in center us germinal center
Germinal Center
Dark zone: young B cell called central blast undergo the somatic hypermutation, produce Ig and selection for higher affinity antibodies.
light zone: B cells interact with T follicular helper cells (Tfh cells), and FDCs (follicular dendritic cells) for further selection and differentiation. B cells here also undergo class switching. to form plasma cells and memory B cell.
Mantle Zone: Navie B cell
Marginal Zone: memory B cell.
paracortex: T cell
medulla: B cell including the Plasma cells
Role: Antigen recognition, Antigen processing, Lymphopoiesis, Act as filters removing foreign particles
When B cells in primary follicles encounter an antigen until they are activated by helper T cells or antigen-presenting cells (APCs)., they migrate to the secondary follicles. This migration leads to the formation of germinal centers, where the B cells undergo proliferation, differentiation, and affinity maturation. and B cells can also undergo class switching (e.g., from IgM to IgG) and somatic hypermutation to improve the affinity of their antibodies for the antigen.
Burkitt's lymphoma
Mantle cell lymphoma
primary cutaneous follicle centre lymphoma.
Follicular lymphoma
HCL - Variant
Splenic marginal zone lymphoma (SMZL)
Hcl,hairy cell leukemia
CLL, variants
Mature B cell lymphomas, most are lymph node based and occur in elderly
CLL
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Non-Hodgkin Lymphomas- NHL
mixed the mature like lymphocyte and prolymphocyte (< 50%). Small and large lymphoid cells
PLL
Prolymphocytic leukemia: majority are prolymphocytes. and major is Bcell. More aggressive.
60 yrs, male
Severe splenomegaly, absent or minimal lymphadenopathy
Prolymphocytes >55% of leukemia cells in PB
CD 19,20,22, FMC7
NegativeL CD 23, 103, 123. Weak or absence:+- CD 5
B cells with abundant cytoplasm and “hairy” cytoplasmic projections, “fried egg” appearance
50-55 yrs, male, involves BM and spleen. ( central to the B cell maturation process and immune function. )
clinical: insidious. Rare lymphadenopathy. BM firbosis "dry tap". d/t the HCL leukemia cells produce and enlarge the function is production fibrogenic. This process leads to a hypercellular bone marrow and impairs normal hematopoiesis, contributing to symptoms like pancytopenia. neutropenia, functional abnoramlities of granulocytes, depressed NK cells, T helper and T suppressor cells. Later hypocellular BM
Lab: dry tap, >=50 hairy cells in PB, hypocellular BM, Tartrate resistant acid phosphatase d/t hairy cell, increase LAP. strong: CD 22,25,79a, 11c, 103 123.
B cell neoplasm replace splenic white pulp. Lympocytes is villous lymphocytes. typically associated with chronic antigen stimulation from infection or autoimmunity. Features: resemble prolymphocytes, and moderately basophilic villous cytoplasm. positive CD 20, 79a, negtaive: cd 5,23,123
average 71 yrs, massive splenomegaly and marked leukocytosis with numerous circulating neoplastic cells. negative CD 25, trap, cd123.
lymph nodes, spleen, BM. germinal centers. 90% t(14;18), sIgG, CD 10,19,20. negative CD 5,23
tumor in head/trunk. BCL 6, CD20, 79a, 10, 19, 22, 38
aggressive lymphoproliferative male elders. Bcell neoplasm of small to medium lymphoid celss with irregular nuclei. lymph nodes
dark zone in the germinal center. variants 1. endemic for young children , jaw bone mass w/EB . 2. sporadic for in children, young adults. abdomianl mass, gonads and breast 3. HIV population immunodeficiency Associated.
t (8,14), t (2,8), t (8,22) , CD 19,20,22,10, BCL-6,CD 38
Large granular lymphocytic leukemia
T cell leukemia-lymphoma
T cell PLL
lymphocytosis, more aggressive, clinical course with lymphadenopathy, spleenomegaly. serious effusions and skin lesions., CD 4 and CD8
RNA retrovirus human T-cell lymphoma- leukemia virus I -- Monoclonal proliferative disorder, Median age, increase LDH
CD2, CD3, CD5, CD4, CD25 (bright), nuclear convolution (flower or clover leaf),
large granular lymphocytes Monoclonal proliferation . CD16, CD56, CD57
(T-LGLL): CD3+, often CD8+, NK type: CD3 negative
B cell in bone marrow to get mature, so BM is primary lymphoid organs.
Minor population: 10%-20%. a lot of Ig on B cell surface membranes. particularly in the form of IgM and IgD
T Cell cLL/PLL
mycosis fungoides: cutaneous lymphoma, skin lesions-- later develop BM, blood circulated-- sezary syndromez
Microscopy: Infiltration of small to medium lymphoid cells with darkly staining and irregular nuclear. Present cerebrum appearance to the nucleus
present CD2, CD3, CD5, CD4, Absence of CD7
sezay: Erythroderma, Generalized lymphadenopathy, Presence of Sézary cells in skin, lymph nodes, and peripheral blood. more aggressive
Lipid storage disorder
Gaucher disease
Neiman pick disease
Sea blue Histiocyte syndrome
eccentric nucleus and foamy cytoplasm, filled with uniformly sized droplets of accumulated lipid. (lot of evaculation.
Spleenomegaly. like fumble tissue paper. deficiency of glucocerebrosidase --increase glucocerebroside accumuated in monocyte/macrophage. "crump tissue paper"
prognosis
Type I: nonneuronopathic
1
Type II:
acute neuronopathic is infant --3
Type III:
subacute neuronopathic is juvenile --2
osteoblasts. only in the Bm