Avian B cells

Detailed studies on the molecular basis of switching in chicken have not yet been published. 

Switching to classes other than IgD is most obvious in activated B cells. Extensive studies have been performed on mouse B cells that have been polyclonally activated by bacterial lipopolysaccharide (LPS) [2,16-18] or by both LPS and switch factors , i.e. certain lymphokines produced by T lymphocytes [6-9]. Antigen stimulation in vitro (e.g. [19]) and mitogenic stimulation of human B cells (e.g. [20]) 

A second type of activated B cell is the memory cell, an obscure cell type defined by its function. The experiment of Okumura et al. [15], in which the IgG2 memory was transferred with sorted surface IgG2+ B cells, is the strongest evidence so far for the notion that memory B cells already switch upon their generation. 

In summary, IgH class switching in mammalian B cells seems to be closely associated with B cell activation and occurs only rarely, if at all, prior to activation. 

Much of the confusion as to when and at what frequency B cells switch stems from the analysis of lymphomas and plasmacytomas. Since such transformed cells can be cloned and adapted to grow in vitro they have been studied extensively. 

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McCormack, W.T., Tjoelker, L.W., Thompson, C.B. (1991). Avian B-cell development generation of an immunoglobulin repertoire by gene conversion. Annu. Rev. Immunol. 9,219-241. 

Lila, D., Susana, Z. Ricardo, B. (1994). Induction of a calbindin-Dgic-like protein in avian muscle cells by 1,25-dihydroxy-vitamin Dj. Biochem. Mol. Biol. Int, 32,859-67. 

In the rat, AgB-associated differences in response to a number of synthetic polypeptide and foreign protein antigens have been described . In the chicken, the B-locus, or a linked genetic factor, has been found to control resistance to Marek s disease (an avian leukosis virus-induced lymphoma), and also to autoimmune thyroiditis . Differences in response to the synthetic polypeptide (T,G)-A-L have also been observed . An extremely interesting observation in the chicken indicates a requirement for shared products of the same MHC haplotype in order for effective T cell—B cell cooperation to take place, as in the mouse. 

Rutowski, R.L. et al.. Pterin pigments amplify iridescent ultraviolet signal in males of the orange sulphur butterfly, CoUa eurytheme, Proc. R. Soc. B, 272, 2329, 2005. Oliphant, L.W., Pteridines and purines as major pigments of the avian iris. Pigment Cell Res., 1, 129, 1987. 

Frykberg, L., S. Palmieri, H. Beug, T. Graf, M.J. Hayman, and B. Vennstrom, Transforming capacities of avian erythroblastosis virus mutants deleted in the erbA or erbB oncogenes. Cell, 1983. 32(1) 227-38. 

Vennstrom B, Bishop JM. Isolation and characterization of chicken DNA homologous to the two putative oncogenes of avian erythroblastosis virus. Cell 1982 28 135-143. 

Granger, B. L., and Lazarides, E. (1982). Structural association of synemin and vimentin in avian erythrocytes revealed by immunoelectron microscopy. Cell 30, 263-275. 

Figure 16.7. Microscopic appearance of necrosis. (A) Coagulative necrosis in a virally infected avian liver. Hepatocytes in the lower half of the photo are in various stages of necrosis, with small, pyknotic or fragmented nuclei and increased cytoplasmic eosinophilia. (B) Necrotic cells in immune-mediated skin disease, canine. The central cell has a pyknotic nucleus and intensely eosinophilic cytoplasm, while the cells at lower left and upper left are injured and swollen. The smaller cells are neutrophils. See color insert.

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