Volume 9, Issue 1, Pages 71-79 (July 1998) Lymph Node Genesis Is Induced by Signaling through the Lymphotoxin β Receptor  Paul D. Rennert, Danelle James, Fabienne Mackay, Jeffrey L. Browning, Paula S. Hochman  Immunity  Volume 9, Issue 1, Pages 71-79 (July 1998) DOI: 10.1016/S1074-7613(00)80589-0

Figure 1 LTβ-R-Specific MAb AF.H6 Has Antiproliferative Activity on Human WiDr Cells WiDr cells were grown for 4 days in the presence (circles) or absence (squares) of 50 U/ml interferon-γ with a control hamster MAb (open) or AF.H6 (closed) at the indicated concentrations. Interferon-γ alone has a slight antiproliferative effect and reduced the absorbance from 1.3 to 0.9. Immunity 1998 9, 71-79DOI: (10.1016/S1074-7613(00)80589-0)

Figure 2 An Agonist LTβ-R-Specific MAb Delivered In Utero Induces LN Genesis in LTα−/− Mice Shown are brachial (A and B) and mesenteric (C and D) LN in adult LTα+/+ mice (A and C) and in 4-week-old LTα−/− mice (B and D) that had been treated with 250 μg of anti-LTβ-R MAb AF.H6 in utero on gestational days 13, 15, and 17. Immunity 1998 9, 71-79DOI: (10.1016/S1074-7613(00)80589-0)

Figure 3 Development of All LN in Wild-Type Mice Can Be Ablated by Embryonic Treatment with Both LTβ-R-Ig and TNF-R55-Ig Fusion Proteins Iliac and sacral LN are present in mice treated in utero with LFA-3-Ig fusion protein (A); sacral LN remain in mice treated in utero with LTβ-R-Ig fusion protein (B) but are absent in mice treated in utero with both LTβ-R-Ig and TNF-R55-Ig fusion proteins (C). BALB/c mice were treated in utero with 100 μg of LFA-3-Ig, 100 μg of LTβ-R-Ig, or 100 μg each of LTβ-R-Ig and TNF-R55-Ig fusion proteins on gd 11, 14, and 17. Immunity 1998 9, 71-79DOI: (10.1016/S1074-7613(00)80589-0)

Figure 4 Embryonic Signaling of LTβ-R Is Insufficient to Establish or Maintain the Cellular Organization within LN Induced to Form in LTα−/− Mice Shown are immunohistochemical analyses of representative brachial LN from LTα+/+ mice (A, C, E, and G) and induced to form in LTα−/− mice (B, D, F, and H). LN were dissected from 4-week-old mice and stained with antibodies to B220 ([A and B], green), CD4 ([A and B], red), PNAd (C and D), sialoadhesin (E and F), and FDCM2 (G and H). Immunity 1998 9, 71-79DOI: (10.1016/S1074-7613(00)80589-0)

Figure 5 Antagonism of the TNF-R55 but Not the LTβ-R Pathway in Normal Adult Mice Disrupts the Maintenance of Cellular Organization in LN Normal adult mice were treated i.p. with purified fusion proteins for 10 days or with MAbs for 7 days starting at 6 weeks of age, and then LN were harvested for analysis of cellular organization in LN. Axillary LN from LFA-3-Ig (A), TNF-R55-Ig (B), LTβ-R-Ig (C), MAb Ha4/8 (D), MAb TN3 (E), and MAb AF.B3 (F) treated normal adult mice were stained with antibodies to B220 (green) and CD4 (red). Immunity 1998 9, 71-79DOI: (10.1016/S1074-7613(00)80589-0)