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Table 9.1 Functional aspects of T and B cells. 
T cells B cells 
Origin Thymus Bone marrow 
Tissue distribution Parafollicular areas of cortex in 
nodes, periarteriolar in spleen 
Germinal centres of lymph nodes, spleen, 
gut, respiratory tract; also subcapsular 
and medullary cords of lymph nodes 
Blood 80% of lymphocytes; CD4 > CD8 20% of lymphocytes 
Membrane 
receptor 
TCR for antigen BCR (= immunoglobulin) for antigen 
Function CD8+: CMI against intracellular 
organisms 
Humoral immunity by generation of 
antibodies 
CD4+: T-cell help for antibody 
production and generation of 
CMI 
Characteristic 
surface markers 
CD1 CD19 
CD2 CD20 
CD3 CD22 
CD4 or 8 CD9 (pre B cells) 
CD5 CD10 (precursor B cells) 
CD6 CD79 a and b 
CD7 HLA class I and II 
HLA class I 
HLA class II when activated 
Genes rearranged TCR α, β, γ, δ IgH, Igκ, Igλ 
BCR, B-cell receptor; C, complement; CMI, cell-mediated immunity; HLA, human leucocyte antigen; Ig, immunoglobulin; 
TCR, T-cell receptor. 
Table 9.2 Some properties of the three main classes of immunoglobulin (Ig). 
IgG IgA IgM 
Molecular weight 140 000 140 000 900 000 
Normal serum level (g/L) 6.0–16.0 1.5–4.5 0.5–1.5 
Present in Serum and 
extracellular fluid 
Serum and other body fluids 
(e.g. of bronchi and gut) 
Serum only 
Complement fixation Usual Yes (alternative pathway) Usual and very efficient 
Placental transfer Yes No No 
Heavy chain (γ1–4) α (α1 or α2) μ
Table 9.3 Causes of lymphocytosis. 
Infections 
Acute: infectious mononucleosis, rubella, 
pertussis, mumps, acute infectious 
lymphocytosis, infectious hepatitis, 
cytomegalovirus, HIV, herpes simplex or 
zoster 
Chronic: tuberculosis, toxoplasmosis, 
brucellosis, syphilis 
Chronic lymphoid leukaemias (see Chapter 17) 
Acute lymphoblastic leukaemia 
Non-Hodgkin lymphoma (some) 
Thyrotoxicosis 
HIV, human immunodeficiency virus. 
Table 9.4 Classification of immunodeficiencies. 
Primary 
B cell (antibody deficiency) X-linked agammaglobulinaemia, acquired common variable 
hypogammaglobulinaemia, selective IgA or IgG subclass deficiencies 
T cell Thymic aplasia (DiGeorge’s syndrome), PNP deficiency 
Mixed B and T cell Severe combined immune deficiency (as a result of ADA deficiency or 
other causes); Bloom’s syndrome; ataxia-telangiectasia; Wiskott– 
Aldrich syndrome 
Secondary 
B cell (antibody deficiency) Myeloma; nephrotic syndrome, protein-losing enteropathy, anti-CD20 
(rituximab) therapy 
T cell AIDS; Hodgkin lymphoma, non-Hodgkin lymphoma; drugs: steroids, 
ciclosporin, azathioprine, fludarabine, etc. 
T and B cell Chronic lymphocytic leukaemia, post-stem cell transplantation, 
chemotherapy/radiotherapy, anti-CD52 (alemtuzumab) 
ADA, adenosine deaminase; AIDS, acquired immune deficiency syndrome; Ig, immunoglobulin; PNP, purine nucleoside 
phosphorylase.

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Chapter09

  • 1. Table 9.1 Functional aspects of T and B cells. T cells B cells Origin Thymus Bone marrow Tissue distribution Parafollicular areas of cortex in nodes, periarteriolar in spleen Germinal centres of lymph nodes, spleen, gut, respiratory tract; also subcapsular and medullary cords of lymph nodes Blood 80% of lymphocytes; CD4 > CD8 20% of lymphocytes Membrane receptor TCR for antigen BCR (= immunoglobulin) for antigen Function CD8+: CMI against intracellular organisms Humoral immunity by generation of antibodies CD4+: T-cell help for antibody production and generation of CMI Characteristic surface markers CD1 CD19 CD2 CD20 CD3 CD22 CD4 or 8 CD9 (pre B cells) CD5 CD10 (precursor B cells) CD6 CD79 a and b CD7 HLA class I and II HLA class I HLA class II when activated Genes rearranged TCR α, β, γ, δ IgH, Igκ, Igλ BCR, B-cell receptor; C, complement; CMI, cell-mediated immunity; HLA, human leucocyte antigen; Ig, immunoglobulin; TCR, T-cell receptor. Table 9.2 Some properties of the three main classes of immunoglobulin (Ig). IgG IgA IgM Molecular weight 140 000 140 000 900 000 Normal serum level (g/L) 6.0–16.0 1.5–4.5 0.5–1.5 Present in Serum and extracellular fluid Serum and other body fluids (e.g. of bronchi and gut) Serum only Complement fixation Usual Yes (alternative pathway) Usual and very efficient Placental transfer Yes No No Heavy chain (γ1–4) α (α1 or α2) μ
  • 2. Table 9.3 Causes of lymphocytosis. Infections Acute: infectious mononucleosis, rubella, pertussis, mumps, acute infectious lymphocytosis, infectious hepatitis, cytomegalovirus, HIV, herpes simplex or zoster Chronic: tuberculosis, toxoplasmosis, brucellosis, syphilis Chronic lymphoid leukaemias (see Chapter 17) Acute lymphoblastic leukaemia Non-Hodgkin lymphoma (some) Thyrotoxicosis HIV, human immunodeficiency virus. Table 9.4 Classification of immunodeficiencies. Primary B cell (antibody deficiency) X-linked agammaglobulinaemia, acquired common variable hypogammaglobulinaemia, selective IgA or IgG subclass deficiencies T cell Thymic aplasia (DiGeorge’s syndrome), PNP deficiency Mixed B and T cell Severe combined immune deficiency (as a result of ADA deficiency or other causes); Bloom’s syndrome; ataxia-telangiectasia; Wiskott– Aldrich syndrome Secondary B cell (antibody deficiency) Myeloma; nephrotic syndrome, protein-losing enteropathy, anti-CD20 (rituximab) therapy T cell AIDS; Hodgkin lymphoma, non-Hodgkin lymphoma; drugs: steroids, ciclosporin, azathioprine, fludarabine, etc. T and B cell Chronic lymphocytic leukaemia, post-stem cell transplantation, chemotherapy/radiotherapy, anti-CD52 (alemtuzumab) ADA, adenosine deaminase; AIDS, acquired immune deficiency syndrome; Ig, immunoglobulin; PNP, purine nucleoside phosphorylase.