Subpopulations of B- And T-Lymphocytes and NK (Natural Killer) Cells (LGL – Large Granular Lymlphocytes) in Patients With Infectious Mononucleosis
DOI:
https://doi.org/10.5644/Radovi.316Abstract
In a group of 54 patients with verified diagnoses of infectious mononucleosis values of leukocytes, lymphocytes and atypical mononuclear cells (AMNC) in the peripheral blood were measured and the number of B-lymphocytes, T11 T4, T8-lymphocytes and large granular lymphocytes (LGL) and NK (natural killer) cells respectively identified and determined by appropriate immunological tests.
Maximal leukocyte values in the peripheral blood did not exceed 14 x 109/1 and were recorded in the first three weeks of the disease. Lymphocytes and AMNC were predominating cells in the differential leukocyte formula. Their maximal values amounted up to 88 percent and were largest in the first three weeks of the disease. The values of antibodies to VCA (viral capsid antigen) and of antibodies to EBNA (Epstein-Barr nuclear antigen) were in accord with data reported in the literature.
In direct immunofluorescence tests (polyvalent and monovalent anti-immunoglobulin antibodies) we found increased values of B-lymphocytes, which culminated in the first week of the disease. In most cases we recorded elevated values of B-lymphocytes which carried on their membranes IgG 4 + IgM + IgA or IgG + IgM. The rise B-lymphocyte values was most likely due to the action of EB virus as polyclonal activator of B-cells resulting in their proliferation and differentiation.
In indirect immunofluorescence tests with use of anti-TH, anti-T4 and anti-T8 monoclonal antibodies we found increased Tll-lymphocytes values and marked rise in the values of suppressor-cytotoxic T-lymphocytes (T8) throughout the entire duration of the disease. There was also a mild upward trend in the values of T-helper lymphocytes (T4). Infection of B-lymphocytes with EB virus was accompanied by intensive immune stimulation and the activation of, and increase in the values of, T-lymphocytes, in the first place of those with a cytotoxic and suppressor function (T8), which also seemed to have been primarily activated. The tendency of a light increase in T-helper lymphocytes (T4) values might have been the result of the activation of this subspecies of T-lymphocytes in acute infectious mononucleosis.
In the smears of whole blood and in the smears of separated lymphocytes, and with the use of monoclonal NKH’ antibodies, we found increased values of large granular lymphocytes (LGL) and NK (natural killer) cells, respectively, which tallies with the results reported by other researchers. The increase in the mean values of NK cells was greatest between the fifteenth and thirtieth days of the disease. An intact function of NK cells is a precondition for normal protection against herpes simplex virus, so that these cells would behave in a similar way also against Epstein-Barr (EB) virus. NK cells alone could directly act on EB virus-infected B-cells, thus immediately taking part in defence processes, and could together with activated cytotoxic T-cells act on the plasma cells whose appearance is the result of virus-induced transformation of B-lymphocytes and could eliminate them. T-suppressor lymphocytes would restrict the growth of EB virus-infected B-cells by acting antiproliferously.
References
Jondal, M. and Klein, G. (1973): Surfacc markers on human B and T lymphocytes. II. Presence of Epstein-Barr virus receptors on B lymphocytes. J. Exp. Med., 138:1365—1378.
Fingeroth, J. D., Weis, J. J., Tedder, T. F., Strominger, J. L., Biro, P. A. and F earon, D. T. (1984): Epstein-Barr virus receptor of human B lymphocytes is the C3d receptor CR2. Proc. Natl. Acad. Sci. (USA), 81:4510—4515.
Frade, R., Barel, M., Ehlin-Hendrikkson, B. and Klein, G. (1985): Gp 140 the C3d receptor of human B lymphocytes, is also the Epstein-Barr virus receptor. Proc. Natl. Acad. Sci. (USA), 82:1490—1493.
Young, L. S., Sixbey, J. W., Clark, D. and Rickinson, A. B. (1986): Epstein-Barr virus receptors on human pharingeal epithelia. Lancet., 1:240—242.
Sixbey, J. W., Vesterinen, E. A., Nedrud, J. G., Raab-Traub, N., Walton, L. A. and Pagano, J. S. (1983): Replication of Epstein-Barr virus in human epithelial cells infected in vitro. Nature, 306:480—489.
Sixbey, J. W., Nedrud, J. G., Raab-Traub, N., Hanes, R. A. and Pagano, J. S. (1984): Epstein-Barr virus replication in oropharyngeal epithelial cells. N. Engl. J. Med., 310:1225—1230.
Sixbey, J. W., Davis, D. S., Young, L. S., Hull-Fletcher, L., Tedder, T. T. and Rickinson, A. B. (1987): Human epithelial cell expression of an Epstein-Barr virus receptor. J. Gen. Virolog., 68:805—811.
Sixbey, J. W., Lem on, S. M. and Pagano, J. S. (1986): A second site for Epstein-Barr virus shedding: The uterin cervix. Lancet, 2:1122—1124.
Klein, E., Ernberg, I., Masucci, M. G., Szigeti, R., Wu, Y. T., Masucci, G. and Svedmyr, E, (1981): T-cell reponse to B-cells and Epstein-Barr virus antigens in infectious mononucleosis, Cancer Res., 41: 4210—4215.
Softić, N. (1988): Hematološke laboratorijske pretrage, Sveučilišna naklada Liber, Zagreb, str. 322.
Kordić, D., Lukač, J., Silobrčić, V., Spaventi, S., Dekaris, D. (1986) :Simple enumeration of large granular lymphocytes. Periodicum Biologorum, 88:248—249. (Supp. 1).
Sheldon, P. J., Papamichail, M., Hemsted, E. H. and Holborow, E. J. (1973): Thymic origin of atipical lymphoid cells in infectious mononucleosis. Lancet, 1:1153—115.
Papamichail, M., Sheldon, P. J. and Hol boro w, E. J. (1974): T and B cell subbpopulation in infectious mononucleosis, Clin. Exp. Immunol., 18:1—11.
Leavell and Thhhorup's (Thorup, O. A. Jr.) Fundamentals of Clinical Haematology (1987). W. B. Sannders Company, Phyladelphia-London-Thoronto, Fifth Ed., str. 72; 469.
Tosato, G., Magrath, L, Koski, I., Dolly, N. and Blaese, M. (1979): Activation of suppressor T-cells during Epstein-Barr virus-induced infectious mononucleosis. N. Engl. J. Med., 301:1133—1137.
Hassan, J., Feighery, C., Bresnihan, B., Whelan, A. (1990): Increased CDS+B cells in patients with infectious mononucleosis. Brit. J. Haematology, 74:375—376.
Tomkinson, B. E., Maziarz, R., Sullivan, J. L. (1989): Characterisation of the T cell-mediated cellular cytotoxicity during acute infectious mononucleosis, J. Immunol., 143:660—670.
Rickinson, A. B. (1986): Cellular immunological response to the virus infection. In the Epstein-Barr virus. Epstein, M. A. and Achong, B. G., eds. John Willey and Sons, New-York, str. 75.
Brewster, F. E., Byron, K. S. and Sullivan, J. L. (1985): Immunoregulation during acute infection with Epstein-Barr virus: Dynamics of interferon and 2'5'-oligoadenylate sinthetase activity. J. Infect. Dis., 151:1109—1115.
Miyawaki, T., Kasahara, Y., Kanegane, H., Ohta, K., Yachic, A. and Taniguchi, N. (1991): Expression of CD45RO(UCHL1) by CHD+ and CD h cells as a sigu of in vivo activation in infectious inonomicleosis, Clin. Exp. Immunol., 83:447—451.
Tomkinson, B. E., Wagner, D._ K., Nelson, D. L. and Sullivan, J. L. (1987): Activated lymphocytes during acute Epstein-Barr virus infection J. Immunol., 139:3802—3807.
Williams, M. L., Loughran, P. Jr., Kidd, P. G. and Starkebaum, G. A. (1989): Polyclonal proliferation of activated suppressor/cytotoxic T cells with transient depression of natural killer cell function in acute infectious niononucleosis, Clin. Exp. Immunol., 77:71—76.
Lopez, C. (1984): Natural resistance mechanistns against herpes virus in health and disease, in Rouse, B. T., Lopez, C. (eds): Immunobiology of Herpes Simple.r Infectious, Boca Raton, F. L. CRC Press, str. 45—64.
Tosato, G. (1989): Cell-mediated immunitv, in Schlossberg, D.: Infectious tnononucleosis, Eds. Springer Verlag, str. 100—116.
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