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passages (Monekton and Moroni 1980) followed by assaying for infectious xenotropic virus. BALB/c x 129 cross es were kindly performed for us by Ms. Hämmerli (Tierfarm Sisseln). All BALB/c mice tested (15/15) were positive by these procedures, while all 129 mice (10/10) were negative. All (BALB/cX 129)F 1 mice resembled BALB/c, i.e., inducibility was dominant. F 1 mice were backcrossed to 129 mice and tested for inducibility by LPS/BrdU; of these, 32160 (53%) showed the BALB/c phenotype, implying that one gene controls induction by LPS/BrdU. Spleen cells from a number of the same mice were also tested for LPS induction. Aperfect correlation was observed between LPS/BrdU and LPS: 17/17 LPS/BrdU positive mice were positive with LPS alone and 15/15 LPS/BrdU negative mice were noninducible with LPS. Induction with LPS and LPS/BrdU seemed, therefore, under the control of the same gene. D. Discussion LPS induction and BrdU "amplification" of endogenous virus production in BALB/c lymphocytes have a number of features in common. In both cases xenotropic virus is produced. Induction is controlled by the same genetic locus, probably the structural gene for BALB virus-2. The finding that BrdU increases the number of infectious centers by a factor of ten more than reverse transcriptase (Table 1) might weIl reflect an increased virus pro ducti on per cell and hence an increased probability of detection. Both processes appear to require cell proliferation and differentiation. This suggests that murine lymphocytes release xenotropic virus at a certain stage along anormal differentiation pathway and that B-cell mitogens induce virus by stimulating the appearance of cells which produce virus. Antibody secretion itself does not appear to be required for virus production, since BrdU amplifies virus while at the same time inhibiting ASe. Incorporation of BrdU into the DNA of three different types of cells derived from BALB/c mice has three different consequences for endogenous virus expression. In fibroblasts xenotropic and ecotropic viruses are induced, in stimulated B-cells xenotropic virus production is amplified, and in stimulated T -cells no infectious virus production occurs. The observation that a-IgM re duces the level of LPS/BrdU induction from B-cells suggests that certain differentiated functions, acquired only late in B-cell differentiation and present in fibroblasts, are required for virus induction. One dass of candidates for this differentiation function are RNA-processing enzymes. The switch from surface to secreted IgM, which takes pi ace after LPS stimulation, is thought to involve an alteration in mRNA processing (Singer et al. 1980). In a manner analogous to the failure of C-type viruses and SV40 to replicate in undifferentiated teratoma cells (Teich et al. 1977; Segal et al. 1979), the absence of the appropriate processing enzymes in T -cells might render them refractory to induction by BrdU. References Anderson J, Bullock WW, Melchers F (1974) Eur J Immunol 4: 715 - Besmer P, Smotkin D, Haseltine W, Far H, Wilson AT, Paskin JM, Weinberg R, Baltimore D (1974) Cold Spring Harbor Symp Quant Bid 39: 1103 - Cohen PL, Scher I, Mosier DE (1976) J ImmunoI116:301- Gronowicz E, Coutinho A, Me1chers F (1976) Eur J Immunol 6:588 - Monckton RP, Moroni C (1980) J Gen Virol 47:59 - Moroni C, Schumann G (1975) Nature 254:60 - Moroni C, Schumann G, Robert-Guroff M, Suter ER, Martin D (1975) Proc Natl Acad Sci USA 72:535 -Moroni C, StoyeJP,DeLamarter JF, Erb P, Jay FA, Jongstra J, Martin D, Schumann G (1980) Cold Spring Harbor Symp Quant Bio144: 1205 - Peebles PT (1975) Virology 67 :288 - Schumann G, Moroni C (1976) J Immunol 116: 1145 - Segal S, Levine Al, Khoury G (1979) Nature 280:335 - Singer PA, Singer HH, Williamson AR (1980) Nature 285:294 -Teich N, Lowy D, Hartley JW, Rowe WP (1973) Virology 51:163 - Teich NM, Weiss R, Martin GR, Lowy DR (1977) Ce1112 : 973 - Wecker E, Schimpl A, Hünig T (1977) Nature 269:598 367
Haematology and Blood Transfusion Vol. 26 <strong>Modern</strong> Trends in Human Leukemia IV Edited by Neth, Gallo, Graf, Mannweiler, Winkler © Springer-Verlag Berlin Heidelberg 1981 Modulation 01 Growth 01 Malignant CeUs by Anti-Idiotypic Immunity H. Schreiber, P. M. Flood, M. L. Kripke, and J. L. Urban A. Introduction One of the mechanisms capable of regulating an immune response involves the inter action of idiotypes and anti-idiotypes. In selected nontumor systems it has been shown that anti-idiotypic immunity can very specifically either suppress or stimulate immune responses (for review see Eichmann 1978). Thus, antiidiotypic reagents may provide powerful tools for manipulating the induction or course of the host's immune responses to malignant cells. To test this hypothesis, we have developed a tumor model in which anti-idiotypic immuni- Immunization of C3H/HeN (MTV-) ~ mice with live ~ 1591 tumor cell, Anti-1591 Iymphoblasts in adjuvant (3x) 3 weeks interval 1 I 5 day culture ~ e f';.';.;"'t'.IV. :~"'\'"' .,1iI\ ! Nonresponding Iymphocytes in adjuvant (3 x) Restimulation of immune spleen cells in vitro with 1591 tumor cells in mixed Iymphocyte-tumor ce" culture BSA equilibrium density centrifugation Adjuvant alone (3x) No treatment Adult thymectomy and 500R Testing of animals in vive by challenge with 10 7 live 1591 or 1316 tumor cells. Other animals analyzed for cytolytic activity and immune responsiveness !!!. vitro. Fig. 1. Experimental protocol used for the generation and purification of tumor-specific lymphoblasts, immunization with these cells, and subsequent testing of blast-immunized and control animals. For details see Flood et al. (1980) 368
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Haematology and Blood Transfusion 2
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Dr. Rolf Neth, Universitäts-Kinder
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Participants of the Meeting Aaronso
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Kurth, R, Friedrich-Miescher-Labora
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Wilsede Scholarship Holders (Grante
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Preface Gut ist eine Lehrart, wo ma
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Personal and scientific discussion
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Acknowledgement We should like to t
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Wilsede, June 21 1978 Memorial Trib
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limiting benign lymphoproliferative
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this most unlikely, however (for re
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longer subject to the same control
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Bregula U, Wiener F, Harris H (1971
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fresh lymph node biopsies from ten
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Fig. 3. Binucleate mitosis in an ob
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y Fig. 4. Schematic diagram of post
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than that among patients with Stage
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Tests of binding affinity, agglutin
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N Engl J Med 297: 963-968 - Green I
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Clinical Aspects
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"ring chromosome". "Mar" is marker,
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191 chromosomally abnormal patients
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tumors of both African and non-Afri
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Haematology and Blood Transfusion V
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Retrospective group 26/93 evolved l
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Treatment
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advantage in terms of duration of f
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leukaemia. An analysis of 168 patie
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11. Treatment Program Chemotherapy
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efractory congestive heart failure
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period (Sequence II) was gene rally
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children with a multiple drug proto
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DAYS 1 5 10 15 20 25 30 35 , I I I
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Biologically Drug Outcome fit" sens
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may counterbalance the potential be
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Ht (0--0) 50 40 30 20 10 0 Platelet
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10 7 ,-----------------------------
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11. Haematological and Biochemical
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0\ 0\ INTERFERON ... 10 3 rl E "'
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("pre-B" phenotype) has been descri
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human bone marrow cells exhibit the
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10 9.,0 MBKCC .. .,4 B prot:oool 1'
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demann W, Büehner T, Arlin Z, Gee
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-...l 00 a-tLDRENS CAt«:ER S TU>Y
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prognostic characteristics under in
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significantly higher in HR} (14.5%,
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normal or elevated immunoglobulin l
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References Andreeff M, Darzynkiewic
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R GROUP 1 ( 1970 - 1971 ) 17 PTS. R
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Table 3. Influence of initial featu
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LIJ (f) a.. < -1 LIJ Q: u. 0 >- I-
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me nt indicated that additional the
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42:2123-2134 - Chessells JM, Cornbl
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Baum et al. 1979). This study was b
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1. 0 '--'1--" 0.9 e: o .- VI VI E C
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e: o e: 1. 0 ,.--...-- 1'"'\ ......
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In conclusion, we can state that th
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Haematology and Blood Transfnsion V
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INDUCTION VCR + PRED + ASNASE (wk 3
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SCHED.INT 1 MTX • ! Adria MTX •
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~ looh---------ooooc>----o---c>----
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Consoll- Irra .tlon t) .tlon Indu
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Highrisk Standard risk Table 1. Cli
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Cumulo/ive comp/el9 remission 1.0 .
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10° 8 = 6 ö 4 Non T Cell .~ :ö
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% SURVIVAL 100 ~ ~II 0 80 60 40 - -
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a) Percentage of donor cell mitoses
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Table 5. Results of bone marrow tra
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...... w N Table 7. Clinical result
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agent had to be added and that in t
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C. Chronic Myelogenous Leukemia The
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Patients with a suitable donor rece
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No. Recurrent Leukaemia Other death
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followed by dialysis against isoton
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HS, HL- Heme >_ 40 0 HS I ;:. =====
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knowing at present. These genes may
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esistance to antifolates. In Vitro
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a DNA probe specific for the gene t
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translocation between chromosomes 9
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Table 1. Subdivision of 1827 Myelo-
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NORMAL CELL ®
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some change of the primary type, in
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F. Transformation of Mouse Bone Mar
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were carried out with 3H-MTX in the
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the lysozyme cDNA prepared from ovi
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et al. 1976). The BJAB cellline in
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dalton bands corresponding to light
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1979). The EBV-carrying cell lines
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producer lines (DAUDI and P3HR-1),
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G, Giovanella B, Westman A, Stehlin
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Dc;bt CT + i J.I9 Raji; 1. i .. 100
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c. Discussion During infectious mon
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C. Nonepisomal Viral DNA We have us
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A 260 3.0 A B 1670 70 N2 2.0 c: E .
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vivo. Nature 260:302-306 - Kirk JTO
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Fig. 1. a Polyacrylamide gelelectro
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1979). The lymphocyte subpopulation
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lysin 0 antigens are found, and mix
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Pope JH (1978) Long-term T cell-med
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Haematology and Blood Transfnsion V
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Charaeteristie Morphologie maturati
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after TPA-induction (Table 3). The
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PA (1978) Reactivity of a rabbit an
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Blood Monocyte. B lood Monocytes 1-
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and nonhistone proteins can serve a
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The findings of the evaluation of s
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Fig. 3. Tumor grawth of L 428 cells
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Cell biological and Immunological A
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consideration. Sanel (1973) obtaine
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endotoxin serum, were used. A parti
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monocytic leukemia cell line in cul
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B. Isolation, Characterization and
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don al hemopathies generally displa
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nitors. Blood Cells 6:595-607 - Min
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\I) ....I ....I IU Jl 200 r 100 90
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their haemopoietic cells' ability t
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normal normal ALL ALL ALL persons p
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64.5 { V)
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References Biermann E, Neth R, Gros
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ehambers, the growth pattern observ
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References Anderssen LC, 10kinen M,
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REH CELL UNE TO CALLb~Ö ~q~ V.M. c
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the macrophage series in which the
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Table 1. Production of factor depen
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Table 1. Characteristics of the adh
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Fig. 3. A human marrow culture at 6
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300 250 • HYPERPROLIFERATIVE PATT
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Fig. 9. Nonadherent population from
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The cobblestone areas were often no
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L (1976) Induction of colony format
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B. Materials and Methods J. Tissue
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Fig. 2. Ultrastructural appearance
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Table 1. Monoclonal antibody reacti
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al. 1979; Janossy et al. 1979) is e
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to which this is an exact replica o
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inger JL (1976) Distribution of la-
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I region antigens were found to be
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have been reported to be present on
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V. FunctionalAssays Assays for PHA
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Functional studies of UCHT1 separat
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Page 327 and 328: 40 ,...... (5 L.. C o u 30 .9 ~ .~
Page 329 and 330: with immunohistochemieal methods (L
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Page 333 and 334: can be dissected by cloning. Utiliz
Page 335 and 336: Table 1. Origin and marker profile
Page 339 and 340: complete identity of gp 100 from no
Page 341 and 342: Table 1. Reaction of single anti se
Page 345 and 346: media. Following 24-h incubation, c
Page 347 and 348: nonleukemic eells (Greaves 1979). L
Page 351 and 352: Fig. 2. Cytocentrifuged smears of b
Page 353 and 354: Modification of amino-groups of hum
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Page 357 and 358: The majority of human blood lymphoc
Page 359 and 360: of the EBV infected B cells. Howeve
Page 361 and 362: and immunoglobulins. J Immunol 120:
Page 363 and 364: " K 10 • j ~ ALL RNlL AL wtfh les
Page 365 and 366: tion akuter Leukämiezellen in "spo
Page 367 and 368: D. Results and Discussion J. Acute
Page 369 and 370: selectively responsive to different
Page 373 and 374: l1J ~ 100 ~ Q. ::) l1J Z 0 ~ z >- .
Page 375 and 376: Table 2. Growth inhibition of S49 e
Page 377: Reverse Infectious ASC/2X1Q6 transc
Page 381 and 382: munized animals to 1316 tumor cells
Page 383 and 384: Haematology and Blood Transfnsion V
Page 385 and 386: Fig. 3. Expression of retroviral gp
Page 387 and 388: pg70. J Exp Med 143: 151-166 - McGr
Page 389 and 390: Table 1. Expression of tumor antige
Page 391 and 392: Virological and Molecularbiological
Page 393 and 394: Table 1. Oncogenic properties of re
Page 395 and 396: also Fig. 1). It followed that the
Page 397 and 398: whether this sequence is related to
Page 399 and 400: zed in infected cells argue that th
Page 401 and 402: a specific viral transforming prote
Page 403 and 404: detect viral RNA as the only charac
Page 405 and 406: Eisen H (1980) Myeloproliferate vir
Page 407 and 408: p,60- -34K - 1 2 3 4 Fig. 1. In vit
Page 409 and 410: .. p - • a'T ... I .t'l Fig. 4. D
Page 413 and 414: Fig. 2. Photomicrographs of NY68 in
Page 415 and 416: DEAE (o(lJmn 'liI GI -2 2 o e s 1
Page 417 and 418: vity was deterrnined. For endogenou
Page 419 and 420: pr 180 - - - P 12/15 - A B c D E F
Page 421 and 422: 85,- 66- -27 - -66 40- 27- -1'9 19-
Page 425 and 426: = 0.5 o E Q. o ILI 0.4 (J) « ILI .
Page 427 and 428: Table 1. Oncogenic potential of avi
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100 III GI c: o "8 80 > w
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Expt. No. Infecting virus Proportio
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Haematology and Blood 'fransfusion
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sequences, provided its gag portion
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77:3009-3013 - Hu SSF, Moscoviei C,
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RI 2.2 md and Hind III 2.6 md leuke
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RELATIONSHIP OF ENDOGENOUS AND EXOG
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E ........ E Cl. U E :::l .... Q) (
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References Astrin S (1978) Endogeno
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the same animal were examined (e.g.
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I) 'IQ a \0 - CL -- Fig. 2. Restrie
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~ ..................... ~ Cell 3' 5
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a :Sa,C! + . ~ 111 i' ( " '~ .J. b
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Table 1 Sampie Tissue TS fragment"
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a b Sac I / rep ._-_.-_ K J nl rep
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Haematology and Blood 'fiansfusion
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Osteopetrosis and osteosarcomas occ
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Lymphoma cellline Table 1. T and B
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Table 2. In vivo growth and oneogen
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Table 1. Transforming aetivity of c
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Table 3. Transformation aetivity of
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- Shoemaker C, Goff S, Gilboa E, Pa
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indieate a shifting of target eell
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Table 2. Expression of Jl and Sourc
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~ i ,..1---------,,':::::::::::::::
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fragment of pBR322 DNA, a 3.0-kbp S
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Mak TW (1979) Proc Natl Acad Sci US
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Table 1. Transformation of 3T3 cell
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inserts in the genome of rapidly tr
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pulations, it seemed likely that th
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contains antigens which react with
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le of reacting in sensitive radioim
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gic approach. In: Hiatt HH, Watson
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12 Eco R [ Fig. 1. Hybridization pa
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10 - '1~ )( -~ S:! E A U I o 1 2
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Haematology and Blood 'fransfusion
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cultures. These cells did not conta
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indication of malignant T-cells in
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Fig. 3. Thin-section electron micro
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Table 3. Lack of detectable related
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J. HTLV Was Present in the Primary
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specific signals into nonspecific s
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Table 2. Distribution of HTLV-relat
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u 10 ~ 20 ~ :c 30 a 40 o Fig. 1. Ki
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SSV TrS-gp labeled effectively with
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60 HFF/SSV cDNA CELL RNAs: 0 HF/SSV
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Antisera a Table 1. Immunofluoresce
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Haematology and Blood 'ftansfusion
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y competition RIA yielded virtually
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SiS'V' gp70: ANTIGEN, ANTI BODY, IM
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type-C virus p30 antigen in cells f
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c. Results The fractionated whole-b
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induced antibodies as well as exper
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- Fig. la-f. Retravirus particles p
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eplication of infecting murine leuk
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immunodeficiency, multic10nal lymph
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Bovine leukemia --, proteins of 499
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Human T- cell - -, characterization
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RNA -, of tumor virus 439 Rous sarc
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Haematology andBlood Transfusion Su
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