Adaptimmune Therapeutics and Noile-Immune Biotech announced that they will co-develop next-generation SPEAR T-cell products, incorporating Noile-Immune's PRIME technology, based upon co-expression of IL-7 and CCL19
. The PRIME technology, which is already being investigated for augmentation of CAR-T cell activity, will be investigated with Adaptimmune's SPEAR T-cells, as part of Adaptimmune's next-generation programs.
Moreover, the noncanonical NF-[kappa]B specific target genes, such as CCL19
(2.0-fold, P < 0.01) and CCL21 (6.5-fold, P < 0.01), were also increased in BDL rats (Figures 3(j) and 3(k)).
The key chemokines directing DCs migration are chemokine (C-C motif) ligand 19 (CCL19
), CCL21, and chemokine (C-X-C motif) ligand 12 (CXCL12) [31, 32].
Based on the functional categorization of chemokines as described by Zlotnik and Yoshie , the elevated chemokines in TS-CONTROL compared to TS-COPD can be classified as follows: Inflammatory (CCL1, 7, and 15; CXCL2 and 9), homeostatic (CCL19
, CCL25), and dual function (CCL17).
CCR7 is a chemokine receptor for CCL19
and CCL21 that is involved in the homing of immune cells to secondary lymphoid organs.
Expression of M1 macrophage markers, including chemokine (C-C motif) ligand 7 (CCL7), CCL19
, CXCL11, indoleamine 2,3-dioxygenase (INDO), and inducible nitric oxide synthase (iNOS), and of M2 macrophage markers, including mannose receptor C-type 1 (MRC1), MAF bZIP transcription factor (MAF), CCL13, filaggrin family member 2 (FLG2), and arginase 1 (ARG1) [41, 42], was analyzed using RT-qPCR.
DCs were allowed to migrate towards chemokine-free RPMI or towards 200 ng/ml CCL19
in RPMI for 3h at 37[degrees]C as described elsewhere .
The chemokine receptor CCX-CKR mediates effective scavenging of CCL19
(2,17) In the peripheral lymph nodes, LFA-1 on T cells is activated when HEV-associated chemokines including CCL21/ CCL19
and CXCL12 interact with their specific receptors on T cells, CCR7 and CXCR4, respectively, whereas LFA-1 on B cells is activated by interactions with CXCL13 via CXCR5.
Additionally, CCR7 and its ligands CCL19
and CCL21 have recently been suggested as another chemotactic axis for MSCs [18, 19].
Chung, "Loss of RUNX3 expression promotes cancer-associated bone destruction by regulating CCL5, CCL19
and CXCL11 in non-small cell lung cancer," The Journal of Pathology, vol.
As expected, imDCs with BTLA overexpression and EGFP controls showed a weak potential for chemotaxis towards CCL19
(also known as MIP-3[beta]), whereas CCR7-overexpressing cells had the strongest migratory ability of the four groups (Figure 4).