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White blood cells

Organisation of the Body

QuestionAnswer
Physiological challenges Do no harm when all is normal Defend rapidly against pathogens Keep defending against persistent pathogens Eliminate self cells that are abnormal Keep a rapid response memory of previously encountered pathogens
White cells <0.2% of blood cells are white 7000 per ul of blood All are CD45+
Types of white blood cell Neutrophils - 62% Lymphocyte - 30% Monocyte - 5% Eosinophils - 2.5% Basophils - 0.75%
Fractionation of white blood cells Tube contains heparin to prevent clotting Spun in a centrifuge Lymphoprep splits cells due to high molecular weight Granulocytes bind to lymphoprep and aggregate so move downwards All other wbcs form a thin layer of monocyte cells
Quantifying leukocyte subsets by flow cytometry Draw blood from subject Separate mononuclear cells using a ficoll gradient Stain with fluorescent antibody conjugates Optimise fluorescence detector sensitivity Pass stained cell suspension through laser beam Gate cell populations of interest
Origins of white cells in haematopoiesis Come from haematopoietic stem cells Antigens are characteristic of each cell type, changing during differentiation All are CD7-
Granulocytes CD15+ phagocytic cells that have specialised lysosomes
Neutrophils - polymorphonuclear cells Phagocytes - modified endocytosis Receptors recognise proteins repeating patterns Dynein used to enclose membrane around pathogen Contains granules e.g. azurophilic
Mobility of neutrophils 1 - respond to chemotactic chemicals e.g. pathogen products and chemokines 2 - adhere to endothelium by low affinity to GAGs and high affinity to ICAM-1 3 - extravasate by breaking down endothelium to enter tissues 4 - kill pathogen and die
Eosinophils Larger than neutrophils Granules cationic - eosinophilic Stain orange pink in eosin due to eosinophil catatonic protein and peroxidases Recruited by T lymphocytes Receptors for IgE antibody Defence against parasites Host damage in allergies + asthma
Basophils Least common leukocyte type Stain with basic dyes Granules contain heparin and histamine Similar to mast cells in tissues Rapidly produce interleukins IL4 and IL13 on activation
Monocytes 5-10% of leukocytes Nucleus often kidney shaped no obvious granules CD14+ Precursor of macrophages in inflamed tissues Not blood cells - macrophages
Lymphocytes Antigen specific, genetic innovators Can proliferate when stimulated Leave blood and enter lymph nodes via High Endothelial Venules Can rearrange their genome - different genes to allow recognition of different antigens
Lymphoid anatomy All lymphocytes arise from haematopoiesis in bone marrow T cell mature in the thymus Lymphocytes encounter antigens in secondary lymphoid organs e.g. lymph nodes, spleen and peyers patches Immune reactions generate more lymphocytes
Natural killer cells Some scattered cytoplasmic granules Defence against renegade cells Patrols body for missing self - absence of cell surface passport molecules Kills suspect cells by secreting toxins Important for fetus to survive as an allograph
B cells CD19+ Capable of secreting antigen binding immunoglobulin Millions of genetically different clones of B cell responding to different antigens Recognising right antigen -proliferation of clone, differentiation to plasma cell, generation of memory cells
T helper cells CD3+ CD4+ CD8- recognise professional antigen presenting cells Specificity - MHC Class II - peptide combination Secrete cytokines that promote or modulate the responses of other cells e.g. IL2
Cytotoxic T cells CD3+ CD4- CD8+ Recognise virus infected cells Specificity - MHC class I peptide complex Secrete toxic granules to site of recognition Kill infected cells
Leukocyte antigen interactions CD4+ helper cell activates B cells It also activates cytotoxic T cells and mature DCs It is stimulated itself by mature DCs This is done by the secretion of cytokines specific for each cell type
Deficiency of T lymphocytes DiGeorge syndrome Deletion of 22q 11.2 leads to loss of thymus development No adaptive immunity - except some thymus independent antibodies No graft rejection
Deficiency of B lymphocytes X linked agammaglobulinemia Mutation in Bruton Tyrosine kinase No antibodies - numerous infections
Deficiency of all lymphocytes Severe combined immunodeficiency Many variants e.g. ADA-SCID lack of adenosine deaminase No adaptive immunity No graft rejection
Deficiency of all phagocytes Chronic granulomatous disease X linked and autosomal recessive - deficiency in phagolysosome killing component Phagocytes fail to kill bacteria - recurrent pyogenic infection
Deficiency of neutrophils Chediak-Higashi syndrome Autosomal recessive - failure to mature granulocytes Neutropenia - recurrent pyogenic infections
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