Immunoglobulins on the Surface of Lymphocytes

F o r reasons not relevant to the present studies, thoracic d u c t l y m p h o c y t e s from y o u n g B A L B / c mice were observed to synthesize an H chain with a different mobility from/~-chain. This finding was unexpected because the H chains synthesized b y and on the surface of splenocytes from similar animals are almost exclusively/z-chain (1). T o investigate this finding further, thoracic duct l y m p h o c y t e s and splenocytes of y o u n g B a l b / c mice were labeled with [3H]tyrosine or were surface radioiodinated with 125I. T h e classes of Ig synthesized and secreted b y these cells and a t t a c h e d to their cell surfaces were determined. Materials and MethodsPreparation of Cell Suspension.--Male Balb/c mice of 21~-3~ mo of age were purchased from Jackson Laboratories, Bar Harbor, Maine. Cell suspensions were prepared from perfused spleens and thoracic duct lymphocytes were obtained (2) from the first 18-24 h of drainage. 6-wk old germ-free mice (C3H) were obtained from Sprague Dawley, Madison Wis.Radiolabding of Cdls.--Cells were iodinated as previously described (1) at a conc'entration of 108 cells/ml with 2 mCi of 126I, 50/zg of lactoperoxldase (Sigma Chemical Co., Inc., St. Louis, Mo.) and 25 #1 of 0.03% hydrogen peroxide. The reaction was terminated after 5-10 rain by the addition of 25 volumes of cold phosphate-buffered saline pH 7.3 (PBS). Cells were centrifuged, washed once in PBS and once in Eagle's Minimal Essential Medium (MEM) (Grand Island Biological Corp., New York).For labe]ing with [3H]tyrosine, cells were washed in MEM containing 10% fetal calf serum and 2% antibiofic-anfimycotic mixture and lacking tyrosine. Cells were suspended at 5 X 10e/m]. 40-100/zCi/ml of L-tyrosine (3,5-3H) (New England Nuclear, Boston, Mass.) were added and the cultures were incubated at 37°C in a moist CO2 environment.

Section: Discussioncontrasting

confidence: 51%

Cell Surface Immunoglobulin

Uhr

Vitetta

1974

“…The core of data presented means nothing else than direct experimental evidence for what has been expressed before by many researchers (18)(19)(20)(21)(22)(23)(24)(25)(26). To quote Mitchison (27) it has to be assumed "that nothing except antibody recognizes antigen, and we must therefore assume that the receptor for antigen is antibody already present at a site, in or on the cell, prior to exposure to antigen."…”

Section: Discussionmentioning

confidence: 99%

Cellular Receptors

Ramseier

Lindenmann

1971

The injection of parental strain lymphoid cells into F1 hybrid animals is known to lead to manifestations of graft-versus-host (GVH) 1 reactions. It is generally agreed that the initiation of this process is set in motion by parental strain cells recognizing transplantation antigens the F1 host has inherited from the other parent (1). This recognition process is assumed to be accomplished by recognition structures (RS) presumably located on the surface of parental strain lymphoid cells. If such a parent-to-F1 GVH reaction is considered from a genetical point of view, it seems reasonable to assume that an F1 animal fails to detect on injected parental strain lymphoid cells any foreignness, with the notable exception of particular recognition structures.It was demonstrated earlier (2-4) that these structures were antigenic. The injection of moderate numbers of parental strain immunocompetent cells into F1 hosts led to the production of anti-recognition structure (anti-RS) antisera. The activity of these sera could be demonstrated by their ability to block the corresponding recognition structures on parental strain cells and thus prevent antigenic recognition. Anti-RS sera have, furthermore, been shown to be of exquisite specificity. Since for genetic reasons an F1 host can be expected to react only against RS which it does not possess, its serum will contain only antibody to the newly introduced parental RS. It could be shown that treatment of a suspension of parental strain lymphoid cells with such an antiserum blocked the RS in question but left RS for other transplantation antigens free to recognize corresponding antigens (3, 4).While these anti-RS sera have all been provoked by injections of low numbers of parental strain lymphoid cells into adult F~ hybrid hosts, the present communication intends to show that similar antibodies can be elicited by a seemingly remote immunization procedure. Instead of considering only immunocompetent cells as bearers of recognition structures for foreign trans-

“…The class of mammalian lymphocytes equivalent to the bursa-derived (B) 1 lymphocytes of birds may be identified by the presence of large amounts of immunoglobulin (Ig) on the surface of most of these cells (1,2). In addition, many of these B lymphocytes, but not thymus-derived (T) lymphocytes, bear a surface receptor for an activated component of C3 allowing them to bind antigen-antibody-complement complexes (3).…”

Section: (From the Laboratory Of Immunology And The Laboratory Of CLImentioning

confidence: 99%

Ontogeny of B Lymphocytes

Gelfand

Elfenbein

Frank

et al. 1974

121

The class of mammalian lymphocytes equivalent to the bursa-derived (B) 1 lymphocytes of birds may be identified by the presence of large amounts of immunoglobulin (Ig) on the surface of most of these cells (1, 2). In addition, many of these B lymphocytes, but not thymus-derived (T) lymphocytes, bear a surface receptor for an activated component of C3 allowing them to bind antigen-antibody-complement complexes (3). These cells are referred to as complement receptor lymphocytes (CRL).Although no functional role for the C receptor of B lymphocytes has yet been established, at least two major possibilities have been suggested. Firstly, the C receptor by binding antigen-antibody-complement complexes may serve as an antigen concentrating mechanism and thus increase the likelihood that antigens would interact with with specific receptors on the surface of immunocompetent B lymphocytes and then activate these cells (4). Alternatively, it has been proposed that B-lymphocyte activation requires the interaction of that cell both with specific antigen and with another ligand leading to the generation of two signals within the cell. A major candidate for the ligand generating the so-called "second signal" would be activated C3 binding to to the C receptor (5). In such a model the binding of activated C3 would be crucial to B-cell stimulation.