Effect of Low-Temperature Plasma-Modified Carbon Fibers on Impact Load Damage of Low-Density Oil-Well Cement.

After large-scale exploitation of conventional oil and gas resources, most remaining resources are in highly depleted zones, where the fracture pressure of the formations is greatly reduced. Low-density oil-well cement prevents wellbore and formation fractures by reducing annular liquid column pressure and is one of the most commonly used cements in the oil and gas industry. However, cement sheaths made of low-density oil-well cement can be easily damaged due to the impact load generated during the well completion process. Incorporating carbon fibers into the cement matrix can effectively enhance the performance of cement sheaths. To ensure that carbon fibers can be closely combined with the cement matrix, low-temperature plasma modification technology was used in this study to pretreat the fibers. The mechanical properties of low-density oil-well cement incorporated with unmodified or modified carbon fibers were studied in detail under an impact load. The results of X-ray photoelectron spectroscopy revealed that the content of hydrophilic groups on the surface increased from 18.3 to 60.3% after the plasma treatment. The impact test results showed that the peak strengths of the cements cured at 60 °C for 14 days with 0.3% unmodified and modified carbon fibers could reach 37.01 ± 1.7 and 62.27 ± 1.7 MPa, respectively, under the impact load, i.e., an increase of 68.25% after the carbon fibers were treated with low-temperature plasma. Similarly, the absorbed energy increased from 15.59 to 44.31 J, and the energy absorption rate increased from 25.98 to 73.85%. Low-temperature plasma modification provided hydrophilic functional groups on the surface, significantly improving the interfacial bonding between the carbon fibers and cement matrix. The strengthened interaction was beneficial to extending the bearing time under the impact load and demonstrated a positive influence on the mechanical properties related to the impact resistance.

CD69 Imposes Tumor-Specific CD8+ T-cell Fate in Tumor-Draining Lymph Nodes.

Tumor-specific CD8+ T cells play a pivotal role in antitumor immunity and are a key target of immunotherapeutic approaches. Intratumoral CD8+ T cells are heterogeneous; Tcf1+ stemlike CD8+ T cells give rise to their cytotoxic progeny-Tim-3+ terminally differentiated CD8+ T cells. However, where and how this differentiation process occurs has not been elucidated. We herein show that terminally differentiated CD8+ T cells can be generated within tumor-draining lymph nodes (TDLN) and that CD69 expression on tumor-specific CD8+ T cells controls its differentiation process through regulating the expression of the transcription factor TOX. In TDLNs, CD69 deficiency diminished TOX expression in tumor-specific CD8+ T cells, and consequently promoted generation of functional terminally differentiated CD8+ T cells. Anti-CD69 administration promoted the generation of terminally differentiated CD8+ T cells, and the combined use of anti-CD69 and anti-programmed cell death protein 1 (PD-1) showed an efficient antitumor effect. Thus, CD69 is an attractive target for cancer immunotherapy that synergizes with immune checkpoint blockade.

The cellular and molecular basis of CD69 function in anti-tumor immunity.

Cancer immunotherapy utilizes our immune system to attack cancer cells and is an extremely promising strategy for cancer treatment. Although immune-checkpoint blockade, such as anti-PD-1 (programmed cell death 1) antibody, has demonstrated significant enhancement of anti-tumor immunity and has induced notable clinical outcomes, its response rates remain low, and adverse effects are always a matter of concern; therefore, new targets for cancer immunotherapy are always desired. In this situation, new concepts are needed to fuel the investigation of new target molecules for cancer immunotherapy. We propose that CD69 is one such target molecule. CD69 is known to be an activation marker of leukocytes and is also considered a crucial regulator of various immune responses through its interacting proteins. CD69 promotes T-cell retention in lymphoid tissues via sphingosine-1-phosphate receptor 1 (S1P1) internalization and also plays roles in the pathogenesis of inflammatory disorders through interacting with its functional ligands Myl9/12 (myosin light chains 9, 12a and 12b). In anti-tumor immunity, CD69 is known to be expressed on T cells in the tumor microenvironment (TME) and tumor-draining lymph nodes (TDLNs). We revealed that CD69 negatively regulates the effector function of intratumoral T cells and importantly controls the 'exhaustion' of CD8 T cells. In addition, we and others showed that either CD69 deficiency or the administration of anti-CD69 monoclonal antibody enhances anti-tumor immunity. Thus, CD69 is an attractive target for cancer immunotherapy.